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Ira Tabas, M.D., Ph.D. Richard J. Stock Professor and Vice-Chairman of Research Department of Medicine Professor of Anatomy & Cell Biology (in Physiology and Cellular Biophysics) E-mail: iat1@columbia.edu Website:http://www.cumc.columbia.edu/dept/medicine/tabas_site/ Office: Room PH 8-East 105F Office Tel: 212-305-9430 Laboratory: Rooms PH 9-405-406 Laboratory Tel: 212-305-5669 |
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CURRENT RESEARCH THE CELLULAR AND MOLECULAR BIOLLOGY OF MACROPHAGES DURING ATHEROGENESIS The laboratory utilizes cell-culture models and induced mutant mice (i.e., transgenics and knockouts) to explore areas of macrophage cellular and molecular biology that are pertinent to the development of atherosclerosis. During atherogenesis, macrophages become loaded with cholesterol ("foam cell" formation), a process that plays a critical role in this disease process. In this context, the laboratory studies basic cellular processes involved in the uptake, intracellular trafficking, metabolism, and cell biological effects of cholesterol. SELECTED PUBLICATIONS Feng B, Yao PM, Li Y, Devlin CM, Zhang D, Harding HP, Sweeney M, Rong JX, Kuriakose G, Fisher EA, Marks AR, Ron D, Tabas I. The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages. Nat Cell Biol. 5, 781-92 (2003). [view pdf] Feng B, Zhang D, Kuriakose G, Devlin CM, Kockx M, Tabas I. Niemann-Pick C heterozygosity confers resistance to lesional necrosis and macrophage apoptosis in murine atherosclerosis. Proc Natl Acad Sci U S A. 100, 10423-8 (2003). [view pdf] Li Y, Ge M, Ciani L, Kuriakose G, Westover EJ, Dura M, Covey DF, Freed JH, Maxfield FR, Lytton J, Tabas I. Enrichment of endoplasmic reticulum with cholesterol inhibits sarcoplasmic-endoplasmic reticulum calcium ATPase-2b activity in parallel with increased order of membrane lipids: implications for depletion of endoplasmic reticulum calcium stores and apoptosis in cholesterol-loaded macrophages. J Biol Chem. 279, 37030-9 (2004). [view pdf] Li Y, Schwabe RF, DeVries-Seimon T, Yao PM, Gerbod-Giannone MC, Tall AR, Davis RJ, Flavell R, Brenner DA, Tabas I. Free cholesterol-loaded macrophages are an abundant source of tumor necrosis factor-alpha and interleukin-6: model of NF-kappaB- and map kinase-dependent inflammation in advanced atherosclerosis. J Biol Chem. 280, 21763-72 (2005). [PDF reprint] Tabas I. Consequences and Therapeutic Implications of Macrophage Apoptosis in Atherosclerosis. The Importance of Lesion Stage and Phagocytic Efficiency. Arterioscler Thromb Vasc Biol. (2005) [PDF reprint] Devries-Seimon T, Li Y, Yao PM, Stone E, Wang Y, Davis RJ, Flavell R, Tabas I. Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor. J Cell Biol. 171, 61-73 (2005). [PDF reprint] Maxfield, F.R., Tabas, I. (2005) Role of cholesterol and lipid organization in disease. Nature 438:36-45. [PDF reprint] |
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