Graduated Research Project Leader Archives - Ocean State Research Institute

Christopher Mantsounga, PhD

admin — Tue, 08 Nov 2022 21:46:38 +0000

Christopher Mantsounga, PhD

Instructor of Medicine (Research)

Providence VA Medical Center/Vascular Research Laboratory (VRL)
Brown University
Box 830 Chalkstone Avenue
Building 35
Box G-VA
Providence, RI 02908

christopher_mantsounga@brown.edu
201-273-7100 ex 4327

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Bio

Dr. Chris Mantsounga is appointed as an Instructor of Medicine (Research) at Brown University Warren Alpert Medical School and affiliate to Ocean State Research Institute (OSRI) at Providence VA Medical Center (PVAMC). Dr. Mantsounga graduated from the University of Paris V Descartes at Paris (France) where he obtained his Ph.D. in Cardiovascular Pathology. He did his postdoctoral fellowship in the Dr. Morrison’s Laboratory at the Rhode Island Hospital and PVAMC. His basic sciences research interests include mechanisms of immune-mediated vascular remodeling focusing on areas where immune cells direct the biologic processes of angiogenesis/arteriogenesis and vascular calcification in diabetic state and age-related defects.

Dr. Mantsounga has approximated 10 years’ experience and expertise in cellular and molecular mechanisms involved in inflammation, new arterial and capillary growth in both tumors and ischemic injury models. Dr. Mantsounga has contributed as first or co-author in high impact journals, including original and review articles (Cells reports 2022; Angiogenesis 2018; Diabetes 2012 etc).

Dr.Mantsounga’s research has been supported and awarded by the French National Research ministry as well as the CardioPulmonary Vascular Biology COBRE Project Leader as a PI. Dr. Mantsounga’s work for Phase II of CPVB/COBRE focuses on the uncoupling IL-1beta/VEGF-A signaling axis in inflammatory arteriogenesis and in the context of aging which could lead to a better understanding of reduced VEGF-A and VEGF-A-mediated downstream signaling pathway while IL-1beta expression is increased in Type 2 diabetes mouse model.

COBRE Abstract

Peripheral artery disease (PAD) caused by atherosclerosis leads to considerable morbidity and mortality throughout the world, in large part, due to tissue damage from both acute and chronic occlusive ischemia. Current treatments are limited to the modification of risk factors and mechanical revascularization by surgical bypass or angioplasty. Preclinical studies have identified mechanisms involving bone marrow derived macrophage (BMDM)-dependent angiogenesis in an inflammation suppressed state, but there is also a role for inflammatory macrophages during acute injury to promote effective angiogenesis. We recently defined a novel IL-1 B-dependent transcriptional regulation of the pro-angiogenic isoform of VEGF-A. Primary macrophages with deletion of IL-1 B demonstrate impaired expression of VEGF-A, and consequently, macrophage IL-1 beta deleted mice have impaired angio/ arteriogenesis. Recent preliminary data identified that VEGF-R2 (relative to VEGFR1) expression is also elevated in the inflammatory M1 state and is associated with elevations in IL-1 beta and VEGF-A. Inhibition of VEGF-R2 signaling led to reduced VEGF-A expression despite stable IL-1 beta levels, suggesting an uncoupling of the relationship between IL-1 beta and VEGF-A. Additional preliminary data demonstrated that aged (52-week-old) mice or mice with experimental diabetes have reductions angio/ arteriogenesis, using a PAD model of femoral artery ligation that involves macrophage-directed blood flow recovery. Combined aging with chronic diabetes led to further reductions in blood flow recovery consequent to impaired angiogenesis. Further BMDMs from aged, diabetic mice demonstrated an uncoupling of IL-1 beta and VEGF-A expression, with modest reductions in IL-1 beta and yet severe and disproportionately reduced VEGF-A expression. VEGF-R2 was decreased in aged, diabetic BMDMs. Uncoupling of macrophage IL-1 beta-VEGF-A signaling contributes to impairment of inflammatory angio/arteriogenesis in the setting of long-term type 2 diabetes. Our study aims seek to define the mechanism whereby VEGF-R2 facilitates IL-1 beta-dependent VEGF-A production and consequent arteriogenesis and to determine the impairments in this pathway caused by aging and long term diabetes with the goal of intervening to recover effective angiogenesis in the appropriate clinical context.

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Tasnim Imran, MD, MPH

admin — Tue, 08 Nov 2022 21:35:31 +0000

Tasnim Imran, MD, MPH

Assistant Professor, Medicine

Warren Alpert School of Medicine
Brown University
Box G-L, 185 Meeting St.
Providence, RI 02912

tasnim_imran@brown.edu

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Bio

Dr. Tasnim F. Imran is a cardiologist and clinical research investigator at the Providence VA Healthcare System, Lifespan Cardiovascular Institute (Rhode Island/Miriam Hospitals), and an Assistant Professor of Medicine at the Warren Alpert Medical School of Brown University. Her clinical expertise includes cardiovascular imaging with a focus on echocardiography and cardiovascular magnetic resonance. She is the director of the cardiac MRI program at the Providence VA Medical Center.

Dr. Imran’s research interests include non-invasive imaging, biomarkers in cardiomyopathies, and cardiovascular disease prevention. She is currently the principal investigator of a study supported by the National Institute of General Medical Sciences Cardiopulmonary Vascular Biology COBRE grant to examine the association of advanced imaging and blood biomarkers with quality of life and functional status in patients with heart failure with preserved ejection fraction. Dr. Imran has co-authored numerous articles in peer-reviewed journals and several book chapters. She is an ad-hoc reviewer for Journal of the American College of Cardiology and JACC Heart Failure. She also serves as a member of the prevention council for the American College of Cardiology.

Dr. Imran earned her medical degree at University of Miami Miller School of Medicine in Florida. She completed an internal medicine residency at Rutgers, New Jersey Medical School. Dr. Imran holds a master of public health degree in clinical effectiveness from Harvard T.H. Chan School of Public Health in Boston. She completed a preventive cardiology fellowship at Brigham and Women’s Hospital and VA Boston Healthcare System/Harvard Medical School, and a cardiovascular medicine fellowship at Boston Medical Center/Boston University School of Medicine.

COBRE Abstract

Heart failure with preserved ejection fraction (HFpEF) is highly prevalent and associated with impaired functional tolerance, quality of life, morbidity and mortality. Although medical advances have led to effective treatments for heart failure with reduced ejection fraction, there are very limited treatment options for treating HFpEF which is now recognized as a heterogeneous syndrome. Therefore, there is a critical need to better understand and identify the underlying pathophysiologic mechanisms associated with HFpEF to identify novel therapeutic targets and for personalizing therapy. Despite having normal ejection fraction, it is increasingly being recognized that the heart is not “normal” in patients with HFpEF. While contemporary clinical assessment provides some information beyond ejection fraction in assessment of cardiac function in patients with HFpEF, there is an unmet need to identify novel biomarkers that associate with known pathophysiologic mechanisms and impaired cardiac function.

Pathophysiological alterations in the heart in HFpEF include cardiac remodeling (hypertrophy and fibrosis) and associated changes in cardiac function (LV diastolic dysfunction, longitudinal LV systolic dysfunction, RV systolic and diastolic dysfunction). Cardiac remodeling includes alterations in myofiber orientation in the ventricles, which in turn impacts both systolic and diastolic function. In parallel, HFpEF is associated with impaired myocardial metabolism and energetics (microvascular dysfunction, ischemia, steatosis, and mitochondrial dysfunction) that have a detrimental impact on cardiac function as well. However, few studies have performed comprehensive non-invasive assessment for these key mechanisms in patients with HFpEF and little is known about how these mechanisms relate to functional capacity and quality of life in HFpEF. Amongst the contemporary imaging techniques, Cardiac Magnetic Resonance Imaging (CMR) stands out as a modality that can perform structural, functional, and metabolic assessment of the myocardium. CMR has emerged as the new gold standard for the assessment of the LV and RV function due to its ability to acquire images in multiple planes and direct measurement of volumes. Additionally, advanced techniques such as magnetic resonance spectroscopy (MRS), and diffusion tensor imaging (DTI) can be used to provide information pertaining to myocardial energetics/metabolism and myocardial fiber orientation, respectively. However, no studies have been performed that comprehensively use these advanced sequences in assessment of patients with HFpEF.

In addition to imaging biomarkers, there are emerging circulating biomarkers and assays of HF that relate to underlying pathophysiological mechanisms such as cardiac remodeling (BNP, endothelin-1, Pentraxin-3, and collagen turnover markers) and mitochondrial dysfunction (long-chain acylcarnitines, platelet and PBMC mitochondrial function). However, it is not known whether these biomarkers correlate with the imaging biomarkers of remodeling (DTI) and energetics (MRS) in patients with HFpEF.

Our overall objective in this proposal is to identify imaging and circulating biomarkers with pathophysiological underpinning that are associated with exercise tolerance and quality of life in patients with HFpEF. We hypothesize that novel imaging biomarkers of cardiac remodeling and energetics will relate to functional capacity, quality of life, and circulating biomarkers in patients with HFpEF.

Specific Aim 1: We will examine the association of imaging biomarkers of myocardial fiber orientation with exercise tolerance and quality of life and circulating biomarkers in patients with HFpEF.

Specific Aim 2: We will investigate the relationship of imaging biomarkers of myocardial energetics with exercise tolerance and quality of life and circulating biomarkers in patients with HFpEF.

The expected outcome of this study is that myocardial fiber orientation and myocardial energetics will be associated with circulating biomarkers and exercise tolerance and quality of life in patients with HFpEF. Correlating these key biomarkers with specific underlying mechanisms of ventricular dysfunction will allow for identification of the dominant pathophysiologic mechanism and personalization of therapy for each patient and pave way for future studies to assess the temporal relationship of these mechanisms in HFpEF and changes in these biomarkers in response to therapy.

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Adeel Abbasi, MD

admin — Tue, 08 Nov 2022 21:22:52 +0000

Adeel Abbasi, MD

Assistant Professor, Medicine

Warren Alpert School of Medicine
Brown University
Box G-L, 185 Meeting St.
Providence, RI 02912

adeel_abbasi@brown.edu

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Bio

Adeel Abbasi, MD, ScM, is an Assistant Professor of Medicine in the Division of Pulmonary, Critical Care and Sleep Medicine at Brown University, and Associate Medical Director of the Lifespan Adult Extracorporeal Life Support Program. His work in the Biomedical Artificial Intelligence Laboratory at Brown University’s Center for Biomedical Informatics aims to study and improve outcomes in patients treated with mechanical circulatory support, including extracorporeal membrane oxygenation (ECMO), by leveraging bioinformatics techniques including machine learning to address crucial knowledge gaps. His current research aims to predict complications including severe hemorrhage and thrombosis in patients treated with ECMO to identify modifiable risk factors.

Dr. Abbasi is a Parker B. Francis Fellow and his work is also supported by the CardioPulmonary Vascular Biology Center of Biomedical Research Excellence (CPVB COBRE) at the Ocean State Research Institute, and the Advance Clinical and Translational Research (Advance-CTR) Program of Rhode Island.

COBRE Abstract

Hemorrhage and thrombosis are the most significant causes of morbidity and mortality in extracorporeal life support (ECLS), and of these complications, stroke and intracerebral hemorrhage are the most devastating. The use of ECLS has exploded, but there is no way to accurately identify patients at risk for these complications. My long-term research goal is to improve outcomes in patients treated with ECLS. I will elucidate critical knowledge gaps using bioinformatics techniques including machine learning, a rigorous, data-driven artificial intelligence methodology ideally suited but yet to be leveraged in ECLS. My central hypothesis is that machine learning applied to ECLS data will identify key and modifiable factors associated with these poor outcomes. I will test these hypotheses by developing and analyzing machine learning models to predict hemorrhage (Aim 1) and thrombosis (Aim 2) within the Medical Information Mart for Intensive Care (MIMIC)-IV dataset, a freely available critical care dataset.

The proposed research is highly innovative and timely given the COVID-19 pandemic, which has been marked by the use of ECLS, thrombotic and neurological complications.

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Corey E. Ventetuolo, MD, MS

admin — Fri, 27 Jul 2018 17:09:24 +0000

Corey E. Ventetuolo, MD, MS

Associate Professor of Medicine, Divisions of Pulmonary, Critical Care & Sleep Medicine and Health Services Policy & Practice

Alpert Medical School of Brown University
Rhode Island Hospital
593 Eddy Street, APC 7
Providence, RI 02903

Tel: 401-444-8410
Corey_Ventetuolo@brown.edu

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Corey E. Ventetuolo, MD, MS is an Associate Professor of Medicine and Health Services, Policy, and Practice at Brown University and Director of Academic Affairs for the Pulmonary, Critical Care and Sleep Division at Brown. She is the Associate Director of the Rhode Island Hospital Pulmonary Hypertension Center and Medical Director of the Adult Extracorporeal Life Support Program. Her work focuses on sexual dimorphism in pulmonary arterial hypertension (PAH) and right ventricular function, hormonal modulation as a treatment strategy, and novel methods of endotyping patients with pulmonary vascular disease. She is also interested in improving quality of care for patients with pulmonary hypertension and those on extracorporeal life support. Dr. Ventetuolo is supported by the American Heart Association and the National Institutes of Health.

COBRE Abstract

Female sex is the best established risk factor for pulmonary arterial hypertension (PAH), implying estrogen has a harmful effect on the pulmonary vasculature. Although women are more likely to develop disease, right heart function (which determines prognosis) and survival appears to be better in women with PAH than in men. These paradoxical observations are as yet unexplained. We believe estrogen-mediated angiogenesis leads to changes in the pulmonary vascular bed but also increases in collateral blood flow in the right ventricle. The aim of this project are to correlate changes in angiogenesis markers (including endothelial progenitor cells and microparticles) with measures of pulmonary and right ventricular function during a normal menstrual cycle, which is characterized by fluctuation in estrogen, in PAH patients and in healthy women. We will study similar markers in post-menopausal women and capture hormonal exposures throughout a woman’s lifetime. Linking sex hormone pathways to angiogenesis and the right ventricle could open new avenues for research into the mechanisms of right heart failure, including promising new treatments that alter hormones in women (and men) with pulmonary vascular disease.

Publications

Ventetuolo CE, Mitra N, Wan F, Manichaikul A, Barr RG, Johnson C, Bluemke DA, Lima JAC, Tandri H, Ouyang P, Kawut SM. Oestradiol Metabolism and Androgen Receptor Genotypes are Associated with RV Function. Eur Respir J 2016 Feb;47(2):553-63. doi: 10.1183/13993003.01083-2015. Epub 2015 Dec 2 PMCID: PMC4831135

Ventetuolo CE, et al.. Higher Estradiol and Lower Dehydroepiandrosterone-Sulfate Levels Are Associated With Pulmonary Arterial Hypertension in Men. Am J Respir Crit Care Med Dec 10, 2015 [Epub ahead of print] 2016 May 15;193(10):1168-75. doi: 10.1164/rccm.201509-1785OC. PMID: 26651504 PMCID: PMC4872665

Aliotta JM, Pereira M, Wen S, Dooner MS, Del Tatto M, Papa E, Goldberg LR, Baird GL, Ventetuolo CE, Quesenberry PJ, Klinger JR. Exosomes induce and reverse monocrotaline-induced pulmonary hypertension in mice. Cardiovasc Res. 2016 Jun 1;110(3):319-30. doi: 10.1093/cvr/cvw054. Epub 2016 Mar 14.PMCID: PMC4872677

Kawut SM, Archer-Chicko CL, DiMichele A, Fritz JS, Klinger JR, Ky B, Palevsky HI, Palmisciano AJ, Patel M, Pinder D, Propert K, Smith KA, Stanczyk F, Tracy R, Vaidya A, Whittenhall ME, Ventetuolo CE. Anastrozole in Pulmonary Arterial Hypertension (AIPH): A Randomized, Double-Blind Placebo-Controlled Trial. Am J Respir Crit Care Med. 2016 Sep 7. [Epub ahead of print] PMID: 27602993

Sex and haemodynamics in pulmonary arterial hypertension.
Ventetuolo CE, Praestgaard A, Palevsky HI, Klinger JR, Halpern SD, Kawut SM.
Eur Respir J. 2014 Feb;43(2):523-30. doi: 10.1183/09031936.00027613. Epub 2013 Aug 15.
PMID: 23949961 [PubMed – in process]

Endothelial microparticles in mild chronic obstructive pulmonary disease and emphysema. The Multi-Ethnic Study of Atherosclerosis Chronic Obstructive Pulmonary Disease study.
Thomashow MA, Shimbo D, Parikh MA, Hoffman EA, Vogel-Claussen J, Hueper K, Fu J, Liu CY, Bluemke DA, Ventetuolo CE, Doyle MF, Barr RG.
Am J Respir Crit Care Med. 2013 Jul 1;188(1):60-8. doi: 10.1164/rccm.201209-1697OC.
PMID: 23600492 [PubMed – indexed for MEDLINE]

The renin-angiotensin system and right ventricular structure and function: The MESA-Right Ventricle Study.
Ventetuolo CE, Lima JA, Barr RG, Bristow MR, Bagiella E, Chahal H, Kizer JR, Lederer DJ, Bluemke DA, Kawut SM.
Pulm Circ. 2012 Jul;2(3):379-86. doi: 10.4103/2045-8932.101657.
PMID: 23130107 [PubMed] Free PMC Article

Plasma endothelin-1 and vascular endothelial growth factor levels and their relationship to hemodynamics in idiopathic pulmonary fibrosis.
Ventetuolo CE, Kawut SM, Lederer DJ.
Respiration. 2012;84(4):299-305. Epub 2012 Aug 3.
PMID: 22869459 [PubMed – indexed for MEDLINE] Free PMC Article
Related citations

Brachial artery diameter and the right ventricle: the Multi-Ethnic Study of Atherosclerosis-right ventricle study.
Dibble CT, Shimbo D, Barr RG, Bagiella E, Chahal H, Ventetuolo CE, Herrington DM, Lima JA, Bluemke DA, Kawut SM.
Chest. 2012 Dec;142(6):1399-405. doi: 10.1378/chest.12-0028.
PMID: 22661452 [PubMed – indexed for MEDLINE] Free PMC Article

Selective serotonin reuptake inhibitor use is associated with right ventricular structure and function: the MESA-right ventricle study.
Ventetuolo CE, Barr RG, Bluemke DA, Jain A, Delaney JA, Hundley WG, Lima JA, Kawut SM.
PLoS One. 2012;7(2):e30480. doi: 10.1371/journal.pone.0030480. Epub 2012 Feb 17.
PMID: 22363441 [PubMed – indexed for MEDLINE] Free PMC Article
Related citations

Sex hormones are associated with right ventricular structure and function: The MESA-right ventricle study.
Ventetuolo CE, Ouyang P, Bluemke DA, Tandri H, Barr RG, Bagiella E, Cappola AR, Bristow MR, Johnson C, Kronmal RA, Kizer JR, Lima JA, Kawut SM.
Am J Respir Crit Care Med. 2011 Mar 1;183(5):659-67. doi: 10.1164/rccm.201007-1027OC. Epub 2010 Oct 1.
PMID: 20889903 [PubMed – indexed for MEDLINE] Free PMC Article

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Peng Zhang, MD, MS

admin — Fri, 27 Jul 2018 17:03:56 +0000

Peng Zhang, MD, MS

Assistant Professor of Medicine Rhode Island Hospital

Alpert Medical School at Brown University
CORO WEST
Providence RI 02903

Tel: 401-444-8541
peng_zhang@brown.edu

CVRC

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Bio

Peng Zhang MD. MS. is the Principle Investigator of the Targeted Project 4 of the CardioPulmonary Vascular Biology COBRE. He is an Assistant Professor of Medicine at Rhode Island Hospital and the Alpert Medical School of Brown University.

Dr. Zhang is a graduate of Shanxi Medical University in China and of University of Rhode Island. After being a physician-scientist for almost 3 years in China, he came to the United States to pursue a career in biomedical science and was appointed Instructor in Medicine in 2008 and Assistant Professor of Medicine in 2010, following his postdoctoral training in the Cardiovascular Research Center of Rhode Island Hospital and the Alpert Medical School of Brown University.

Dr. Zhang has a diverse background in medicine and cellular and molecular biology. His research interests concentrate on cardiac remodeling, with a particular focus on cardiac fibroblasts and their role and regulation in the normal and diseased heart. Cardiac remodeling (defined as changes in size, shape and function of the myocardium in response to stress) is a common feature in many cardiovascular and pulmonary diseases including hypertension, coronary artery disease, inflammation, pulmonary arterial hypertension and chronic obstructive pulmonary disease. It can impair ventricular function, increase the risk for arrhythmias and often leads to heart failure. While fibroblasts are important cellular targets for treatment of cardiac remodeling, efforts to develop the treatments for cardiac remodeling that specifically target fibroblasts are still at an early stage. The long-term goals of his studies are to advance understanding of the signaling mechanisms that determine cardiac fibroblast function and to devise new therapeutic strategies for cardiac remodeling that ultimately should benefit patients with cardiopulmonary vascular disease.

Dr. Zhang’s work has been supported by Medical Research Grant from Rhode Island Foundation (2010-2011), a Pilot Project Award (2011-2013) from NIH COBRE for Perinatal Biology, and a Seed Fund Award (2013-2014) from NIH COBRE Center for Cancer Signaling Networks. Recently, Dr. Zhang was awarded by the American Heart Association a National Scientist Development Grant (2013-2016), which aims to support highly promising beginning scientists in their progress toward independence. Furthermore, the Targeted Investigator Project that Dr. Zhang was awarded from the CardioPulmonary Vascular Biology COBRE (2013-2018) significantly enhances the research scope in his laboratory and allows him to be able to compete for a NIH R01 grant soon. Dr. Zhang also contributes as a co-investigator in a R01 project on the regulation of Gq signaling in cardiac fibroblasts (2013-2017).

In addition, Dr. Zhang serves as Ad hoc reviewer for many peer-reviewed journals. He also actively participates in teaching at Rhode Island Hospital and Brown University: he serves as a trainer in the MPP (Molecular Pharmacology and Physiology) graduate program of Brown University, participates as a Junior Faculty trainer in a T32 CardioPulmonary Research Training grant, and participates as a mentor in a T35 Research Training grant.

COBRE Abstract

Regulation of Cardiac Fibroblast Function by MicroRNAs

Fibrosis is an integral feature of the structural remodeling in the heart that occurs in response to a variety of cardiopulmonary diseases and can be a consequence of endothelial injury. It can impair ventricular function, increase the risk for arrhythmias and often leads to heart failure. Cardiac fibroblasts become activated in response to many forms of stress and play a critical role in fibrosis development. They are therefore important therapeutic targets, but therapies that specifically target fibroblasts are still at an early stage. Compared to traditional drug targets, microRNAs (miRNAs) offer novel mechanistic possibilities. Despite rapidly increasing insights into their roles in the heart, the understanding of miRNAs in physiological and pathophysiological processes is just emerging. Several miRNAs are known to regulate myocyte hypertrophy, excitation, contraction and survival; yet very little is known about their role in cardiac fibroblasts. The long-term goal of the miRNA research in my laboratory is to gain a better understanding of the functional role and mechanisms of action of miRNAs in cardiac fibroblasts under physiological and pathophysiological conditions. The central hypotheses of this study are (1) that miRNAs are dynamically regulated upon fibroblast activation and thereby regulate cardiac fibroblast function and (2) that miRNA manipulation in cardiac fibroblasts can be leveraged to prevent and/or reverse cardiac fibrosis development. The significance of the proposed study derives from mechanistic explorations that will provide comprehensive insights into miRNA alterations in cardiac fibroblasts in response to stress and to advance our understanding of the functional role and mechanisms of action of key miRNAs in cardiac fibroblasts, which may provide new opportunities for the treatment and prevention of cardiac fibrosis.

Jacob Moeller, BS, Research Assistant
Nedyalka (Nelly) Valkov, BS, MS, Brown University MPP Program PhD Student

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Joanne Lomas-Neira, PhD

admin — Fri, 27 Jul 2018 16:46:58 +0000

Joanne Lomas-Neira, PhD

Assistant Professor of Surgery (research)

Rhode Island Hospital
Alpert Medical School at Brown University
Dept. of Surgical Research
593 Eddy Street
Aldrich 244
Providence, RI 02903

Tel: 401-444-7796
Joanne_Lomas-Neira@brown.edu

CVRC

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Joanne Lomas-Neira, PhD is an Assistant Professor of Surgery in the Department of Surgical Research at Rhode Island Hospital and a Junior Investigator funded through the CardioPulmonary Vascular Biology COBRE.

Dr. Lomas-Neira is a graduate of the University of Rhode Island receiving undergraduate degrees in Business and Microbiology, a Masters degree in Cytopathology and PhD in Cell/Molecular Biology. Dr. Lomas-Neira did her post-doctoral work in the lab of Dr. Alfred Ayala at Rhode Island Hospital and received her Assistant Professor faculty appointment from Alpert School of Medicine at Brown University in 2013.

Dr. Lomas-Neira received The Rhode Island Foundation award and a Surgical Infection Society Junior Faculty Fellowship. She has 11 first author and 20 co-authored publications. Her work focuses on the roles of angiopoietins 1 and 2 in endothelial and neutrophil activation in the development of Acute Lung Injury. Dr. Lomas-Neira is currently preparing an Ro1 application for independent funding.

COBRE Abstract

Effects of Angiopoietins on shock/sepsis- induced acute lung injury

Acute Lung Injury (ALI) is a complication of trauma characterized by increased microvascular permeability, edema, inflammation, and neutrophil accumulation in the lung. Despite advances in supportive care, trauma patients who develop ALI, still face the risk of significant mortality. While neutrophils have been implicated as playing an important role in the pathogenesis of ALI, vascular endothelial cells (ECs), through their exposure/responsiveness to mediators present in the systemic environment, are also critical to the development of ALI. Using a murine model of hemorrhage (shock) in combination with a subsequent septic challenge, our laboratory has shown that neutrophil interactions with resident pulmonary cells are central to the development of trauma-induced ALI. EC activation, as in vessel remodeling and adhesion and migration of inflammatory cells, is an adaptive response, regulating vascular homeostasis and host defense, respectively. However, the loss of EC barrier function in ALI results in accumulation of fluid, proteins and inflammatory cells within the lung and in compromised gas exchange. This transition from adaptive activation to maladaptive/dysfunction occurs in association with unresolved inflammation. Under normal physiological conditions, regulated expression of two EC effector proteins, Angiopoietins (Ang)-1 & 2 mediates blood vessel formation, remodeling and EC interaction with inflammatory cells. Ang-1 & 2 bind to a tyrosine kinase receptor, Tie2, expressed on endothelial cells (EC). Ang-1 is produced by pericytes, smooth muscle cells, and fibroblasts and is found on the extracellular matrix. Ang-1/Tie2 binding promotes vessel integrity and downstream pro-survival and anti-inflammatory signaling. Ang-2 is stored preformed in EC Weibel-Palade bodies (storage vesicles) and is rapidly released upon EC activation. Unlike Ang-1, binding of Ang-2 plays a role in vascular remodeling and increased vessel permeability. The development of mice over-expressing or deficient in either Ang-1 or 2 has enabled a closer examination of the relationship between these two proteins and their regulation of EC function. Additionaly, it has been proposed that the relative expression of Ang-1 to Ang-2 determines EC responsiveness. In patients that develop ALI plasma Ang-2 levels are significantly elevated. Our recent findings show that Ang-2 is similarly elevated in lung tissue and plasma from mice following shock, in combination with a subsequent septic challenge. Importantly, neutropenic mice do not exhibit this increase. In addition, we have demonstrated that Ang-1:Ang-2 is significantly decreased in mouse lung tissue following shock/sepsis. This decreased ratio is also evident in bronchoalveolar lavage fluid from surgical and trauma ICU patients with ALI suggesting that the altered expression of these two proteins is either predictive or diagnostic of lung injury. However, the actual role Ang-2 plays in shock-induced priming for ALI and regulation of Ang-2’s release/expression has not been examined. To address this, the following central hypothesis is presented:
Angiopoietin-2 promotes loss of pulmonary endothelial barrier function in ALI resulting from the sequential insults of hemorrhagic shock and sepsis and this dysfunction is initiated by EC interaction with activated (shock primed) neutrophils.

Three aims are proposed to test this hypothesis. In Aim 1 we will determine the kinetics of change of Ang-1:Ang-2 in lung tissue and plasma following hemorrhagic shock and/or subsequent septic challenge and assess the role of Ang-1:Ang-2 in the development of ALI and mortality associated with multiple organ failure. This data will be used in Aim 2 to target Ang-1:Ang-2 at selected time points to determine the mechanisms by which Ang-2 changes receptor/adhesion molecule expression and loss of pulmonary endothelial barrier function in mice. In Aim 3 we will determine the degree to which direct EC/PMN interaction regulates the release of Ang-2 and the effects of changes in Ang-1:Ang-2. The data from the proposed study will begin to describe the mechanisms by which PMN-associated, Ang-2-mediated, EC activation leads to ALI. These results are anticipated to provide novel insights into the relationship between the role of angiopoietins in regulating vascular angiogenesis and PMN/EC interactions in the pathogenesis of ALI.

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Qing Lu, DVM, PhD

admin — Fri, 27 Jul 2018 16:39:01 +0000

Qing Lu, DVM, PhD

Associate Professor of Medicine (research)

Providence VA Medical Center
Alpert Medical School of Brown University
830 Chalkstone Ave
Building 35, Room 206
Providence, RI 02908

Tel: 401-273-7100 x3865
Qing_Lu@Brown.edu

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Bio

Dr. Qing Lu, D.V.M., Ph.D. is Associate Professor of Medicine at Alpert Medical School of Brown University and Research Biologist at Providence VA Medical Center. Dr. Lu’s research focuses on lung endothelial biology and innate immunity in cigarette smoke-associated pulmonary diseases, particularly acute respiratory distress syndrome (ARDS), emphysema and pulmonary artery hypertension (PAH). Dr. Lu’s research is currently funded by NIH Ro1. She was also the Principal Investigator (PI) of the project 1 of the CPVB COBRE grant and the PI of several other projects funded by the American Thoracic Society (ATS)/Pulmonary Hypertension Association, the American Lung Association, the Francis Family Foundation, and the Rhode Island Foundation. Dr. Lu has published 50 manuscripts/review articles/ book chapters.

Dr. Lu has served as ad hoc member of NIH study sections (RIBT and LCMI), Department of Defense PRMRP Scientific Peer Review Panels, American Heart Association Peer Review Panels, ATS Peer Review Panels, and several international funding agencies. She is an Academic Editor of journal PLOS ONE and an ad hoc reviewer for many prominent journals. She is currently a member of the Pulmonary Circulation (PC) Planning Committee of ATS and the President of Chinese-America Lung Association. Dr. Lu has served as a member of the Medical Faculty Executive Committee of Brown University in the last 3 years and the Chair of the Institutional Animal Care and Use Committee (IACUC) and the Associate Chair of the Subcommittee for Research Safety (SRS) at Providence VA Medical Center in the last 6 years. As a mentor for various training programs, Dr. Lu has mentored students ranging from undergraduates, graduate students and medical students to pulmonary fellows and post-doctoral fellows. Currently, she serves as a mentor for Dr. Hongwei Yao, a junior investigator of Phase II of the CPVB COBRE. Dr. Lu has taught several courses, including Physiology and Principle of Biology.

COBRE Abstract

Plasma adenosine is increased in patients with sepsis-induced acute lung injury (ALI) and the levels of plasma adenosine correlate with poor survival. Human and mice with adenosine deaminase (ADA) deficiency display progressive lung injury and respiratory distress, suggesting that sustained elevated adenosine is detrimental to the lungs. Our preliminary data demonstrate that prolonged cigarette smoke (CS) exposure increases lung adenosine and exacerbates ALI in mice. We also show that sustained adenosine exposure causes lung endothelial cell (EC) barrier dysfunction via nucleotide transporter (ENT1/2)-dependent, oxidative stress-mediated p38 activation and mitochondrial dysfunction. Thus, we hypothesize that sustained elevated adenosine contributes to CS-primed ALI via ENT1/2-mediated mitochondrial dysfunction and resultant increase permeability pulmonary edema. The long-range goal is to develop novel therapeutic approaches to prevent and treat lung diseases associated with sustained increased adenosine and CS exposure. Specific Aim 1 will determine whether ENT1/2 and mitochondrial oxidative stress mediate increased permeability pulmonary edema in ADA deficient mice and CS-primed ALI mice. Specific Aim 2 will identify the mechanism of deleterious effects of sustained elevated adenosine on mitochondrial function and barrier function of cultured lung EC. These studies will elucidate a novel pathway of adenosine effects mediated by intracellular uptake of adenosine. Inhibition of ENT1/2-facilitated adenosine transport and/or mitochondrial dysfunction may likely provide significant and greatly needed new approaches to treat lung diseases associated with sustained elevated adenosine and CS exposure.

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Sean Monaghan, MD

admin — Fri, 13 Jul 2018 15:32:46 +0000

Sean Monaghan, MD

Sean F. Monaghan, MD, FACS

Assistant Professor of Surgery

Rhode Island Hospital
Middle House 211

smonaghan@lifespan.org
sean_monaghan@brown.edu

Faculty Page

Bio

Sean F. Monaghan, MD, FACS, is an Assistant Professor of Surgery at Brown University and a member of the Division of Trauma and Surgical Critical Care and the Division of Surgical Research. His research attempts to understand the biology of RNA splicing in critically ill trauma and surgical patients using Acute Respiratory Distress Syndrome (ARDS) as a model disease. He uses both human samples and animal models as well as large data sets (GTEx) with computation and molecular biology techniques in his research. Dr. Monaghan has been supported by American College of Surgeons C. James Carrico Faculty Research Fellowship and the National Institutes of Health as a Pilot Project and the Principal Investigator for Project 5 of the CardioPulmonary Vascular Biology Center of Biomedical Research Excellence.

COBRE Abstract

Acute respiratory distress syndrome (ARDS) is a fatal critical illness with mortality rates remaining greater than twenty percent despite numerous clinical trials. It is therefore essential to better understand the basic mechanisms underpinning its development. ARDS is also unique in that it is a common pathway that occurs after many disease processes that result in critical illness (shock from trauma or sepsis, burns, pancreatitis). As such, ARDS represents an ideal model disease to understand severe critical illness and will studied in the proposed animal and human studies. ARDS is characterized by vascular permeability leading to edema and accumulation of immune cells in the lung. The increased vascular permeability is in part due to dysfunction of endothelial cells and will therefore be the focus of this project. Much work has focused on gene expression and evaluation of the protein levels with little emphasis on changes in RNA splicing. RNA splicing is a basic molecular function that occurs in all cells directly after RNA transcription, but before protein translation in which introns are removed and exons are joined together. Over 90% of human genes with multiple exons have alternative splicing events. With such a high rate of variation from the transcribed gene to the produced protein, splicing must be under exquisite control, particularly in times of critical illness. Numerous proteins are involved in the control of RNA splicing, one of interest is U1-70K. Preliminary data suggests that in the lung there is no difference in gene expression, but rather multiple sites of alternative splicing of U1-70K. This is similar to previous work showing that critical illness (ARDS) leads to alternative splicing of membrane bound proteins resulting in a soluble form. We hypothesize that alternative splicing seen during critical illness alters the protein isoforms of U1-70K in endothelial cells. This change in the isoforms, in turn, results in the microvascular permeability and sequestration of edema and immune cells in the lungs during ARDS. With a better understanding of alternative RNA splicing, the long term goal is to manipulate this mechanism to improve outcomes or better predict resolution or ARDS.

Publications

Project Updates

Mentors

William Fairbrother, PhD
Assistant Professor of Biology
Molecular Biology, Cell Biology, & Biochemistry
William_Fairbrother@brown.edu
https://vivo.brown.edu/display/wfairbro

Elizabeth Harrington, PhD
Associate Dean for Graduate and Postdoctoral Studies in the Division of Biology and Medicine, Professor of Medicine
elizabeth_harrington@brown.edu
https://vivo.brown.edu/display/eoharrin

Alfred Ayala, PhD
Professor of Surgery (Trauma) (Research)
alfred_ayala@brown.edu
https://vivo.brown.edu/display/aayalaph

Funded Research

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Jessica Plavicki, PhD

admin — Fri, 13 Jul 2018 15:29:03 +0000

Jessica Plavicki, PhD

Assistant Professor for the Department of Pathology and Laboratory Medicine

Brown University
70 Ship Street
Providence, RI 02903

Tel: (401) 863-6112
jessica_plavicki@brown.edu

Faculty Page

Bio

My lab consists of a team of developmental biologists and environmental scientists working together to understand how genetic mutations and exposure to environmental health contaminants impact brain and heart health. During my undergraduate education and training at the University of Texas at Austin, I developed an appreciation for the importance of utilizing multiple levels of analysis in research to form an integrative understanding of biological processes. As a graduate student in Neuroscience at the University of Wisconsin at Madison, I received training in developmental biology, Drosophila developmental genetics, and biological imaging. My training in developmental biology and a long-standing interest in environmental health science lead me to seek training in toxicology during my next career phase. As a post-doc, I began working with a vertebrate model and extended my training to include zebrafish (Danio rerio) genetics, toxicology, and cardiovascular development. My laboratory at Brown University uses the zebrafish model to study the genetics of brain and cardiovascular development because it provides several distinct advantages. Zebrafish embryos are fertilized externally and develop in an aqueous environment. Passive oxygen diffusion from the environment is sufficient to support embryonic development in the absence of a heartbeat. Consequently, zebrafish embryos with mutations that significantly disrupt cardiovascular development are able to survive and be studied, whereas these mutations would be lethal in a mammalian model. In addition, zebrafish embryos are transparent, which enables us to assess embryonic cardiac function and visualize cardiovascular development in vivo. Despite these critical advantages, the system has yet to be fully exploited to study cardiomyocyte and pharyngeal arch artery development. As a PI, I am committed to increasing diversity in environmental health sciences. I have engaged in outreach activities since early graduate school and will continue to be involved outreach efforts throughout my career. I believe diversity fosters creative, paradigm shifting science.

COBRE Abstract

Congenital heart and great vessels are the leading cause of infant mortality and morbidity in the United States yet the etiology of most congenital defects remains unknown. Approximately 80% of congenital heart and vessel defect cases are multifactorial and exposure to environmental contaminants is thought to significantly contribute to the incidence of defects as well adult heart disease. Our long-term goal is to identify therapeutic targets to treat congenital defects and heart disease by identifying the molecular targets of genes critical for cardiovascular development that are also disrupted by exposure to environmental contaminants. We have identified a candidate gene, SOX9, that is expressed in multiple cell types in the developing and mature heart and is downregulated in animal models following exposure to environmental toxicants present in air pollution, e-waste, plastics, and pesticides. Human mutations in the SOX9 coding region result in Campomelic Dysplasia (CD), a severe genetic disorder that usually results in death. A number of different congenital heart and great vessel defects have been reported in patients with CD as well as in individuals with mutations affecting SOX9 function. Together, the human loss of function data suggests that SOX9 plays several critical roles in cardiac and great vessel development. However, its functions in cardiomyocyte and great vessel development have not been investigated using animal models. Our preliminary data indicate that zebrafish sox9b is essential for cardiomyocyte development and function as well as great vessel formation. Our immediate goal is to identify the molecular mechanisms that mediate the cardiac and great vessel phenotypes observed following loss of sox9b function in zebrafish and to determine if sox9b functions are conserved by mammalian Sox9. We are using an innovative multi-species approach and a combination of genetic tools to manipulate zebrafish sox9b and murine Sox9 during cardiovascular development. In Aim 1.1, we will determine if sox9b is an inhibitor of canonical WNT signaling in the developing zebrafish heart. In Aim 1.2, we will inhibit sox9b function in embryonic cardiomyocytes and use RNAseq to identify additional molecular targets of sox9b during zebrafish heart development. In Aim 2, we use the cell-type specific manipulations and optogenetics to determine how loss of sox9b function leads to the great vessel phenotypes and to determine the relationship between sox9b and two known mediators of great vessel development, nkx2.5, and stat4. In Aim 3, we will extend our understanding of sox9b function in cardiac development by examining how loss of Sox9 in mouse cardiomyocytes and endothelial cells affects cardiac and great vessel development as well as how loss of Sox9 in the murine heart impacts canonical WNT signaling. Together, these studies will help generate critical data that will contribute to our understanding of cardiovascular development and provide putative molecular targets for the development of novel therapeutics to treat congenital heart and vessel defects.

Publications

Project Updates

Mentors

Funded Research

COMPLETED GRANT SUPPORT

1K99ES023848 (Role: PI)
09/01/2014-08/31/2016
9.0 calendar months

NIH/NIEHS
Ahr2 activation and sox9b function in forebrain and cerebral vascular development

The major goals of this project are to: (1) Test the hypothesis that TCDD exposure disrupts development of the zebrafish brain and cerebral vasculature, (2) Determine in which cell types Ahr2 activation produces brain and cerebral vasculature phenotypes, and (3) Test the hypothesis that downregulation of sox9b mediates the TCDD-induced forebrain and cerebral vascular defects.

CURRENT GRANT SUPPORT

R00ES023848-05 (Role: PI)
02/01/2019-01/31/2020
6.0 calendar months

NIH/NIEHS
Ahr2 activation and sox9b function in forebrain and cerebral vascular development

P20GM103652-06 (Role: Project Leader)
07/20/2018-05/31/2020
3.0 calendar months

OSRI COBRE
CPVB COBRE: Project 4: sox9b function in cardiomyocyte and great vessel development

The major goals of this project are to: (1) Identify the downstream targets of sox9b in the zebrafish heart, (2) Determine how loss of sox9b target gene expression disrupts zebrafish great vessel development, and (3) Determine how loss of sox9 target gene expression affects cardiomyocyte and great vessel development in the mouse.

MRI-1919870 (Role: Co-Investigator)
NSF: High resolution mass spectrometer (HRMS) with ultra-high-performance liquid chromatograph (UHPLC)

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Alan Morrison, MD, PhD

admin — Fri, 13 Jul 2018 15:26:01 +0000

Alan Morrison, MD, PhD

Assistant Professor of Medicine at the Warren Alpert Medical School of Brown University

Providence VA Medical Center
Research (151)
830 Chalkstone Ave.
Building 35, room 232
Providence, RI 02908

Tel: 401-273-7100 x6326
alan_morrison@brown.edu

Faculty Page

Bio

Alan R. Morrison, M.D., Ph.D. is Principle/Junior Investigator on CPVB COBRE project “IL-1β Signaling Promotes Atherosclerotic Calcification and Cardiovascular Risk”. He is also a cardiologist at the Providence VA Medical Center He is also a cardiologist at the Providence VA Medical Center with a VA Career Development Award and Assistant Professor of Medicine at the Alpert Medical School of Brown University.

Dr. Morrison is a graduate of the University of Massachusetts at Amherst and the University of Massachusetts Medical School, where he obtained a combined M.D./Ph.D. in Biomedical Sciences. He trained in Internal Medicine at Yale University School of Medicine and Yale New Haven Hospital and did a Cardiovascular Medicine Fellowship at Yale University School of Medicine. In addition, Dr. Morrison received training and certifications in advanced cardiovascular imaging, including Nuclear Cardiology and Cardiac CT. Upon completion of his clinical training, he returned to the research bench and completed a postdoctoral research fellowship in vascular biology under the mentorship of Dr. Jeffrey Bender at Yale. Dr. Morrison was appointed to Assistant Professor of Medicine at Yale School of Medicine in 2014. He was appointed to Assistant Professor of Medicine at Alpert Medical School of Brown University in 2016.

Dr. Morrison has combined careers in clinical cardiovascular medicine, teaching, and vascular biology research. He maintains a strong interest in developing basic research projects that have translational impact for clinical disease. Basic science research interests include mechanisms of immune-mediate vascular remodeling focusing of areas where macrophages direct the biologic processes of arteriogenesis, vascular calcification, and pulmonary arterial hypertension. His laboratory has a number of active studies defining novel macrophage-dependent signaling mechanisms that modulate these processes, using a diverse array of techniques in molecular biology, immunobiology, small animal genetics, and vascular biology.

The goal of Dr. Morrison’s project is to define cellular specific upregulation of the expression of key inflammasome signaling components, IL-1β, IL-1R and IL-1R signaling components, as well as an osteogenic gene program in atherosclerotic plaques as they begin to calcify.

Example: MicroCT Angiogram of New Artery Growth

COBRE Abstract

Coronary artery disease from calcific atherosclerosis is the leading cause of morbidity and mortality in the world. The calcium composition of atherosclerotic plaque has predictive value in terms of cardiovascular events. Inflammation is likely a key mediator of vascular calcification, but immune signaling mechanisms that promote this process are minimally understood. Recently, the inflammatory cytokine, IL-1β, was identified to be increased in calcifying atherosclerotic aortas from ApoE-/- background mice fed a high fat diet. Moreover, plaque and serum from mice with progressive calcification demonstrated increased expression of IL-1β. Treatment with the IL-1 receptor antagonist inhibited atherosclerotic calcification. IL-1β expression was a key driver of vascular smooth muscle cell calcium deposition by its ability to promote expression of the osteogenic transcription factors, RUNX2, SOX9, OSX and MSX2. Bone marrow transplantation confirmed that progressive calcification of plaque is attributable to the hematopoietic compartment. Several key questions remain: 1) are macrophages the key cellular source of plaque IL-1β during atherosclerotic calcification; 2) do vascular smooth muscle cells take on an inflammatory phenotype to promote plaque IL-1β expression; 3) what are the effects of IL-1 receptor signaling on both plaque macrophages and vascular smooth muscle cells; 4) how does IL-1 receptor signaling lead to an osteogenic gene program; and 5) can IL-1β serve as a biomarker of progressive calcification in patients with coronary artery disease. Preliminary data demonstrated that macrophages appear associated with expression of IL-1β in plaque, and consequently, IL-1β signaling through its receptor may play an autocrine positive feedback role in promoting further IL-1β expression by macrophages. Vascular smooth muscle cells, in contrast, appear to play a responsive role to IL-1β signaling by activating an osteogenic gene program. However, global deletion of the IL-1 receptor demonstrated conflicting data about whether nonspecific inhibition of IL-1β signaling can protect against plaque vulnerability, indicating further study to delineate cell-specific contributions in this pathway is required. The hypothesis is that macrophage expression of IL-1β in atherosclerotic plaque and consequent vascular cell IL-1 receptor signaling lead to inflammatory atherosclerotic calcification resulting in increased risk of plaque rupture. Aim 1 will define macrophage IL-1β expression as the critical to inflammatory atherosclerotic calcification. Aim 2 will determine the respective roles of macrophage and smooth muscle cell IL-1 receptor signaling in inflammatory atherosclerotic calcification and osteogenic transcription factor expression. Aim 3 will validate serum IL-1β as a critical biomarker of progressive coronary artery calcification in patients. Confirming that a macrophage IL-1β signaling axis is a central mechanism in inflammatory atherosclerotic calcification in preclinical and translational studies paves the way for developing a novel therapeutic strategy aimed at treating risk in coronary artery disease, as anti-IL-1β therapies have been developed and are actively under investigation.

Publications

Complete List of Dr. Morrison’s Published Work in MyBibliography:
http://www.ncbi.nlm.nih.gov/sites/myncbi/alan.morrison.1/bibliography/47842564/public/?sort=date&direction=ascending

Recent Manuscripts:
A.R. Morrison, T.O. Yarovinsky, B.D. Young, F. Moraes, T.D. Ross, N. Ceneri, J. Zhang, Z.W. Zhuang, A.J. Sinusas, R. Pardi, M.A. Schwartz, M. Simons, J.R. Bender, “Chemokine-coupled beta2 integrin-induced macrophage Rac2-Myosin IIA interaction regulates VEGF-A mRNA stability and arteriogenesis,” The Journal of Experimental Medicine 211 (10): 1957-1968, September 1, 2014.

G. Bailey, J. Meadows, A.R. Morrison, “Imaging Atherosclerotic Plaque Calcification: Translating Biology,” Current Atherosclerosis Reports 2016 August;18(8):51.

N. Ceneri, L. Zhao, B.D. Young, A. Healy, S. Coskun, H. Vasavada, T.O. Yarovinsky, K. Ike, R. Pardi, L. Qin, L. Qin, G. Tellides, K. Hirschi, J. Meadows, R. Soufer, H.J. Chun, M. Sadeghi, J.R. Bender, A.R. Morrison. Rac2 Modulates Atherosclerotic Calcification by Regulating Macrophage Interleukin-1beta Production. Arteriosclerosis, thrombosis, and vascular biology. 2016.

Project Updates

Mentors

Gaurav Choudhary, MD
Associate Professor of Medicine, Alpert Medical School of Brown University Acting Associate Chief of Staff (Research) Providence VA Medical Center
gaurav_choudhary@BROWN.EDU
https://vivo.brown.edu/display/gchoudha

Frank Sellke, MD
Chief of Cardiothoracic Surgery at the Alpert Medical School of Brown University and Rhode Island Hospital
fsellke@lifespan.org
https://vivo.brown.edu/display/fsellke

Funded Research

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