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 Bysani Chandrasekar, D.V.M., Ph.D.Associate Professor Department of Medicine Division of Cardiology
Educational Background:
Areas of Research Interest: Dr. Chandrasekar's laboratory has been studying the role and expression of proinflammatory cytokines and CXC chemokines in myocardial ischemia-reperfusion injury and myocardial failure. At present, Dr. Chandrasekarís laboratory is involved in assessing the role of neutrophils, neutrophil chemoattractants, chemokine and chemokine receptor expression and regulation, and defining the signal transduction pathways involved in cytokine and chemokine mediated myocardial depression and injury. In addition, the laboratory is studying cytokine and chemokine inter-relations, and analysis of chemokine promoters and regulation. Selected Publications: Colston J, Boylston WH, Feldman MD, Jenkinson CP, de la Rosa S, Barton A, Trevino R, Freeman GL, Chandrasekar B. Interleukin-18 plays a causal role in pressure-overload hypertrophy. Biochem Biophys Res Commun. 2007; 354: 552-558. Bhattacharya A, Chandrasekar B, Rahman MM, Banu J, Kang JX, Fernandes G. Inhibition of inflammatory response in transgenic fat-1 mice on a calorie-restricted diet. Biochem Biophys Res Commun. 2006; 349: 925-930. Patel DN, Bailey SR, Gresham JK, Schuchman DB, Shelhamer JH, Goldstein BJ, Foxwell BM, Stemerman MB, Maranchie JK, Valante AJ, Mummidi S, Chandrasekar B. TLR4-NOX4-AP-1 signaling mediates lipopolysaccharide-induced CXCR6 expression in human aortic smooth muscle cells. Biochem Biophys Res Commun. 2006; 347: 1113-1120. Chandrasekar B, Mummidi S, Mahimainathan L, Patel DN, Bailey SR, Imam SZ, Greene WC, and Valante AJ. Interleukin-18-induced human coronary artery smooth muscle cell migration is dependent on NF-KB- and AP-1-mediated matrix metalloproteinase-9 expression, and is inhibited by Atorvastatin. J Biol Chem. 2006; 281: 15099-15109. Perez LE, Chandrasekar B, Saldarriaga OA, Zhao W, Arteaga LT, Travi BL, Melby PC.Reduced Nitric Oxide Synthase 2 (NOS2) Promoter Activity in the Syrian Hamster Renders the Animal Functionally Deficient in NOS2 Activity and Unable to Control an Intracellular Pathogen. J Immunol. 2006; 176: 5519-5528. Chandrasekar B, Valente AJ, Freeman GL, Mahimainathan L, Mummidi S. Interleukin-18 induces human cardiac endothelial cell death via a novel signaling pathway involving NF-κB-dependent PTEN activation. Biochem Biophys Res Commun. 2006; 339: 956-963. Chandrasekar B, Mummidi S, Valente AJ, Patel DN, Bailey SR, Freeman GL, Hatano M, Tokuhisa T, Jensen LE. The pro-atherogenic cytokine interleukin-18 induces CXCL16 expression in rat aortic smooth muscle cells via MyD88, interleukin-1 receptor-associated kinase, tumor necrosis factor receptor-associated factor 6, c-Src, phosphatidylinositol 3-kinase, Akt, c-Jun N-terminal kinase, and activator protein-1 signaling. J Biol Chem. 2005; 280: 26263-26277. Chandrasekar B, Mummidi S, Claycomb WC, Mestril R, and Nemer M. Interleukin-18 is a pro-hypertrophic cytokine that acts through a phosphatidylinositol 3-kinase- phosphoinositide-dependent kinase-1-Akt-GATA4 signaling pathway in cardiomyocytes. J Biol Chem. 2004. 280: 4553-4567. Chandrasekar B, Marelli-Berg FM, Tone M, Bysani S, Prabhu SD, and Murray DR. ß-adrenergic stimulation induces interleukin-18 expression via ß2-AR, PI3K, Akt, IKK, and NF-KB. Biochem Biophys Res Commun. 2004; 319: 304-311. DeGraffenried LA, Chandrasekar B, Friedrichs WE, Donzis E, Silva J, Hidalgo M, Freeman JW, Weiss GR. NF-KB inhibition markedly enhances sensitivity of resistant breast cancer tumor cells to tamoxifen. Ann Oncol. 2004; 15: 885-890. Chandrasekar B, Vemula K, Surabhi RM, Li-Weber M, Owen-Schaub LB, Jensen LE, Mummidi S. Activation of intrinsic and extrinsic pro-apoptotic signaling pathways in Interleukin-18-mediated human cardiac endothelial cell death. J Biol Chem. 2004; 279: 20221-33. Contact Information: Divison of Cardiology University of Texas Health Science Center Phone: 210-567-4598 Fax: 210-567-6960 chandraseka@uthscsa.edu |
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