• Ph.D. Graduate Student; Department of Biotechnology; Jadavpur University (1999)• M.S; Biophysics, Molecular Biology and Genetics; Calcutta University (1993)• B.S; Physiology, Chemistry and Zoology; Calcutta University (1991)
Selected as early stage reviewer to CSI-NIH, 2014• National Scientist Development Award by American Heart Association, 2013• BGIA grant in Aid Award by American Heart Association, 2013• Reviewer for American Heart Association, 2013• Elsa Albrecht Award (1st place) by Cleveland Clinic for outstanding publication, 2006• Travel Award winner from The American Society for Biochemistry and Molecular Biology • Junior Investigator Award finalist in The North American Vascular Biology meeting, 2006 • Awarded 2nd place in the poster competition in Research Day, 2005, Cleveland Clinic• 2nd place in the poster competition in Gordon Conference on “atherosclerosis”, 2005• Awarded Research Fellowship by Government of India for Ph.D. thesis work• Awarded Scholarship for Bachelor of Science examination by Government of India
• Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland (2011-2014)• Research Associate, Department of Cell Biology, Lerner Research Institute (2004-2011)Cleveland Clinic, Cleveland• Post-doctoral Fellow, Department of Cancer Biology, Lerner Research Institute,Cleveland Clinic, Cleveland (2000-2004)• Post-doctoral Scientist, Department of Neuroscience, Indian Institute of Chemical Biology (1999-2000)
The Rahaman Lab is interested in elucidating the molecular signaling events underlying the pathogenesis of various inflammatory diseases, specifically, atherosclerosis and fibrosis. With our studies we hope to gain novel mechanistic insights into pathogenesis of inflammatory diseases, identify potential therapeutic targets, and discover basic molecular and cellular mechanisms of inflammation.ATHEROSCLEROSIS: Cardiovascular disease is the leading cause of death in United States, and atherosclerosis is the most important underlying pathology. The current paradigm defines atherosclerosis as a chronic inflammatory process that results in part by accumulation of modified LDL (oxLDL) in the arterial wall, migration of monocytes to the arterial intima, and formation of lipid-laden macrophage “foam cells”. The earliest atherosclerotic lesion (fatty streak) is primarily composed of macrophage foam cells. A crucial step in foam cell formation is recognition and internalization of oxLDL by scavenger receptors (SR), including CD36 and SR-A. Over the last several years, our group has contributed significantly to the development of important concepts in the field of oxLDL/SR signaling and to understanding the molecular basis of the regulation of foam cell formation (Rahaman et al. Cell Metabolism, 2006-Cover page; Rahaman et al. JBC, 2011-March; Rahaman et al. JBC, 2011-Oct; Rahaman et al. ATVB, 2013, Blood, 2011). Our recently published work has identified Vav-family guanine nucleotide exchange factors (Vav) as critical molecular links that couple hyperlipidemia with pro-atherogenic macrophage responses.Our further work on CD36/oxLDL led to the discovery that Vav regulates macrophage foam cell formation via regulation of Ca2+-initiated signals. On-going experiments are focused on studying Vav mechanisms of action utilizing a multipronged approach involving cells from null mouse strains, in vivo and in vitro assay systems, intravital microscopy, and mouse models of atherosclerosis.FIBROSIS: Fibrosis is the common pathway in virtually all forms of chronic organ failure, including kidney, liver, lung, and heart failure. Patient and animal model studies have revealed that pathological fibrosis requires the presence of numerous mediators of inflammation, chronic tissue injury, and the subsequent generation of myofibroblasts. However, the mechanisms that drive this mesenchymal cell phenotype remain to be elucidated. Emerging data from our group (Rahaman et. al. J Clin Invest, 2014) and others support a role for Ca2+-initiated signals in myofibroblast differentiation. Our objectives are to identify the molecular components of these pathways and to understand how fibroblasts differentiate into myofibroblasts in response to injury and inflammation. On-going experiments are focused on studying how Ca2+ influx in fibroblasts affects fibrogenesis. Using in vivo and in vitro measurements of Ca2+ flux, high throughput Flipper assay, atomic force microscopy, traction force microscopy, fluorescent imaging techniques, and various genetic/molecular/physiological approaches, the Rahaman lab investigates how Ca2+-elicited signaling regulate fibrogenesis.
Rahaman SO*, Grove LM, Paruchuri S, Southern BD, Abraham S, Niese KA, Scheraga RG, Ghosh S, Thodeti CK, Zhang DX, Moran MM, Schilling WP, Tschumperlin DJ, Olman MA*. TRPV4 mediates myofibroblast differentiation and pulmonary fibrosis in mice. J. Clin Invest, 2014 Nov 3. pii: 75331. doi: 10.1172/JCI75331. [Impact Factor: 13.8](* Corresponding author)• Grove LM, Southern BD, Jin TH, White KE, Paruchuri S, Rahaman SO, Gladson CL, Ding Q, Chapman HA, Olman MA. Urokinase receptor (u-PA) ligation induces a raft-localized integrin signaling switch that mediates the hypermotile phenotype of fibrotic fibroblasts. J Biol Chem. 2014, 289(18):12791-804. [Impact Factor: 4.65]• Rahaman SO*, Li W, Silverstein RL*. Vav guanine nucleotide exchange factors regulateatherosclerotic lesion development in mice. Arterioscler Thromb Vasc Biol, 2013, 33(9):2053-7. [Impact Factor: 6.3](* Corresponding author)• Ding Q, Cai G, Hu M, Yang Y, Zheng A, Tang Q, Gladson CL, Hayasaka H, Wu H, You Z, Southern BD, Grove LM, Rahaman SO, Fang H, Olman MA. FAK-Related Non-Kinase Is a Multifunctional Negative Regulator of Pulmonary Fibrosis. Am J Pathol. 2013, 182(5):1572-84. [Impact Factor: 5.2]• Rahaman SO*, Swat W, Febbraio M, Silverstein RL*. Vav family Rho guanine nucleotide exchange factors regulate CD36-mediated macrophage foam cell formation. J Biol Chem.2011, 286(9):7010-7. [Impact Factor: 4.65](* Corresponding author)• Chen K, Li W, Major J, Rahaman SO, Febbraio M, Silverstein RL. Vav guanine nucleotide exchange factors link hyperlipidemia and a prothrombotic state. Blood. 2011, 117:5744-50.[Impact Factor: 9.8]• Rahaman SO*, Zhou G, Silverstein RL*. Vav GEF regulates CD36-mediated macrophage foam cell formation via calcium and dynamin-dependent processes. J Biol Chem. 2011, 286(41):36011-9. [Impact Factor: 4.65](* Corresponding author)• Rahaman SO, Lennon DJ, Febbraio M, Podrez EA, Hazen SL, Silverstein RL. A CD36-dependent signaling cascade is necessary for macrophage foam cell formation. Cell Metabolism (cover page), 2006, 4(3):211-221. [Impact Factor: 16.7]
Rahaman SO, Vogelbaum MA, Haque SJ. Aberrant Stat3 signaling by IL-4 in malignant glioma cells: involvement of IL-13Ralpha2. Cancer Research. 2005, 65:2956-63.[Impact Factor: 9.2]• Ghosh MK, Sharma P, Harbor PC, Rahaman SO, Haque SJ. PI3K-AKT-mTOR signaling pathway negatively controls the EGFR-mediated activation of Stat3 in glioblastoma cells. Oncogene. 2005, 24:7290-7300. [Impact Factor: 8.6]• Rahaman SO, Harbor PC, Chernova O, Barnett GH, Vogelbaum MA, Haque SJ. Inhibition of constitutively active Stat3 suppresses proliferation and induces apoptosis in glioblastoma multiforme cells. Oncogene. 2002, 21:8404-8413. [Impact Factor: 8.6]• Rahaman SO, Sharma P, Harbor PC, Aman MJ, Vogelbaum MA, Haque SJ. IL-13R(alpha)2, a decoy receptor for IL-13 acts as an inhibitor of IL-4-dependent signal transduction in glioblastoma cells. Cancer Research. 2002, 62:1103-1109. [Impact Factor: 9.2]• Rahaman SO, Ghosh S, Mohanakumar KP, Das S, Sarkar PK. Oxidative damage and altered neurofilament gene expression in vivo in hypothyroid rat brain. Neuroscience Research. 2001, 40:273-279. [Impact Factor: 2.3]• Rahaman SO, Ghosh S, Mandal SK, Sarkar PK. Reduced expression and altered distribution of neurofilaments in neurons cultured in thyroid hormone-deficient medium. NeuroReport. 2000, 11(12):2717-2722. [Impact Factor: 1.6]
Ghosh S, Rahaman SO, Sarkar PK. Regulation of neurofilament gene expression by thyroid hormone in the rat brain. NeuroReport. 1999, 10(11):2361-2365. [Impact Factor: 1.6]