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Biography

Shaik O. Rahaman, PhD, is an Assistant Professor in the Department of Nutrition and Food science at the University of Maryland, USA. His laboratory is interested in elucidating the molecular signaling events underlying the pathogenesis of various inflammatory diseases, specifically, atherosclerosis and fibrosis. Dr. Rahaman earned his PhD in Molecular Biology at Jadavpur University, and a BS in Human Physiology (Honors), and an MS in Biophysics and Molecular Biology from University of Calcutta. From 2000-2014, Dr. Rahaman worked at Cleveland Clinic, Cleveland, USA, as a Postdoctoral Fellow, eventually as a Project Scientist studying signal transduction in Cell Biology and Oncology. He has received many awards and honors. Dr. Rahaman was honored with Elsa Albrecht Award by Cleveland Clinic, which is awarded for outstanding publication. During 2011-2014, Dr. Rahaman also served as an Assistant Professor at Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, USA. In 2013, he was the recipient of the American Heart Association Scientist Development Grant. Dr. Rahaman is the author or co-author of 20 research papers on neurobiology, oncology, atherosclerosis, or fibrosis in high impact international peer-reviewed journals of repute including Cell Metabolism and Journal of Clinical Investigation. Dr. Rahaman has given numerous invited talks nationally and internationally, and is a reviewer/editorial board member in numerous scientific journals. Dr. Rahaman also served as a reviewer for National Institute of Health (USA).

Abstract

Cardiovascular disease is the number one cause of death in developed world, and atherosclerosis, a chronic inflammatory arterial disease, is the most dominant underlying pathology. Macrophages are thought to orchestrate atherosclerosis by generating lipid-laden foam cells and by secreting inflammatory mediators. Emerging data support a role for a mechanical factor, e.g., matrix stiffness, in regulation of macrophage function and atherogenesis. We have obtained evidence that TRPV4, an ion channel in the transient receptor potential vanilloid family and a known mechanosensor, is the likely mediator of oxidized low-density lipoprotein (oxLDL)-dependent macrophage foam cell formation, a critical process in atherogenesis. Specifically, we found that: i) genetic ablation of TRPV4 or pharmacologic inhibition of TRPV4 activity by a specific antagonist blocked oxLDL-induced macrophage foam cell formation, and ii) TRPV4 deficiency prevented matrix stiffness or scratch-induced exacerbation of oxLDL-induced foam cell formation. Mechanistically, we found that: i) plasma membrane localization of TRPV4 was sensitized to the increasing level of matrix stiffness, and ii) TRPV4 activity regulated oxLDL uptake but not its internalization in macrophages. Altogether, these findings identify a novel role for TRPV4 in regulating macrophage foam cell formation by modulating uptake of oxLDL.

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