NMH/Arkes Family Pavilion Suite 600
676 N Saint Clair
Chicago IL 60611
Description of Interests
Our research interest focuses on the role of acetyltransferase p300, a major epigenetic regulator, in collagen synthesis and organ fibrosis. Fibrosis, an abnormal matrix remodeling, is a common end-stage pathological symptom of a wide spectrum of vascular injury related multi-organ diseases such as systemic sclerosis, hypertension induced heart and renal failure, myocardial infarction, liver cirrhosis and Idiopathic pulmonary fibrosis. Excessive synthesis and deposition of extracellular matrix proteins especially Type I collagen in the tissues causes fibrosis and eventually organ failure. Transforming growth factor-beta (TGF-b) plays a pivotal role in organ fibrogenesis. We have previously demonstrated that acetyltransferase p300 is essential for profibrogenic cytokine TGF-beta-induced matrix protein collagen synthesis, and TGF-beta induces the levels of p300 in fibroblasts. Most importantly, the levels of p300 are significantly elevated in myofibroblasts derived from resident fibroblasts or vascular endothelial cells and different fibrotic tissues. We are interested to determine i) the molecular basis of p300 elevation in fibrotic tissues, ii) the contribution of elevated level of p300 in cardiac fibrogenesis, iii) the role of p300 in endothelial-to-mesenchymal transition (EndMT) and contribution of EndMT-derived myofibroblast-like cells in cardiac fibrogenesis, and iv) to develop novel therapeutic approaches targeting acetyltransferase p300 to control cardiac fibrosis. We are testing the therapeutic efficacy of a novel small molecule inhibitor of acetyltransferase p300 for prevention and reversal of cardiac fibrosis in two murine models of cardiac fibrosis.
Aging; Cardiovascular Diseases; Epigenetics; Fibrosis; Hypertension; MicroRNA; Signal Transduction; TGF-beta
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