Dr. Qing Lu, D.V.M., Ph.D. is Associate Professor of Medicine (Research) 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 pulmonary diseases associated with cigarette smoke and adenosine signaling. The overall goal of her research is to advance understanding of lung diseases, particularly acute respiratory distress syndrome (ARDS), emphysema and pulmonary artery hypertension (PAH) and to develop novel therapeutic strategies to effectively treat lung diseases. Dr. Lu is the Principal Investigator (PI) of project 1 of the CPVB COBRE grant and the PI of several other funded research grants from the American Thoracic Society (ATS)/Pulmonary Hypertension Association, the American Lung Association, the Francis Family Foundation, and the Rhode Island Foundation.
Dr. Lu is the adviser of several undergraduate research training awards including UTRA and SRA from Brown University. Dr. Lu also serves as the Co-Investigator on multiple funded extramural grants, including two RO1 and three VA Merit Review grants. Dr. Lu has published 38 manuscripts/review articles/ book chapters and 40 abstracts, co-authored with collaborators and students both inside and outside of Brown University. Because of her significant contributions to her research area, she has been frequently invited to present her work at local, national and international forums and conferences. She has also served as a member of peer-review panels for several national and international funding agents, including the ATS, the American Heart Association, the Qutar National Research Fund, and the Medical Research Council of the United Kingdom. She also serves as an Ad hoc peer reviewer for numerous distinguished scientific journals. Additionally, she has served as the Session Chair, Lead Facilitator, and Program Committee Member for the ATS International Annual Conference and other meetings.
Dr. Lu is a member of the training faculty of the Brown University Pathobiology Graduate Program, CardioPulmonary Research Training Program, Brown Undergraduate Summer Research Program, Alpert Medical Student Summer Research Program, and Brown Leadership Alliance Undergraduate Summer Research Program. She has had the privilege of mentoring students ranging from undergraduates, graduate students and medical students to pulmonary fellows and post-doctoral fellows. Dr. Lu has taught Physiology, Principle of Biology and other courses as a lead or guest lecturer for graduate and undergraduate students inside and outside of Brown University. As a valuable citizen of Providence VA Medical Center, Dr. Lu has been organizing research conferences and serving as the Chair of Institutional Animal Care and Use Committee (IACUC) and the Vice-Chair of Subcommittee for Research Safety (SRS) at Providence VA Medical Center.
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.
Two manuscripts related to the Specific Aim 2 have been published on this project. Other proposed studies are ongoing.
Alfred Ayala, PhD
Professor of Surgery
Rhode Island Hospital
Ocean State Research Institute
Providence VA Medical Center
830 Chalkstone Avenue
Providence RI 02908
Research Funded by
Research reported in this website was supported by the National Institute of General Medical Science of the National Institutes of Health under grant number P20GM103652.