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Faculty Detail    
Name JANUSZ H KABAROWSKI
 
Campus Address BBRB 334 Zip 2170
Phone 205-996-2082
E-mail janusz@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Microbiology  Microbiology Associate Professor
Secondary  Pathology   Pathology Chair Office Assistant Professor
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Associate Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Associate Professor
Center  Medicine  Comprehensive Diabetes Ctr Associate Professor
Center  Medicine  Ctr Cardiovasc Bio Associate Professor

Biographical Sketch 
Janusz H.S. Kabarowski received his B.Sc. degree in Biochemistry from University College London, UK. He was awarded a Ph.D. degree from the Leukaemia Research Fund centre at The Institute of Cancer Research (Chester Beatty Laboratories) in London in 1997. Dr. Kabarowski subsequently conducted postdoctoral research in the laboratory of Owen Witte at UCLA. Dr. Kabarowski joined the Department of Microbiology at UAB as an Assistant Professor in 2003 and has a secondary faculty appointment in the Department of Pathology, Division of Molecular and Cellular Pathology.

Research/Clinical Interest
Title
Lipids and lipoprotein metabolism in chronic inflammatory disease
Description
Dr. Kabarowski’s research program is focused on the study of lipids and lipoprotein metabolism in chronic inflammatory disease (notably atherosclerosis and autoimmune disease). Early work characterized the role of the G2A lipid receptor in atherosclerosis and lipoprotein metabolism, showing that pro-atherogenic effects of this receptor may be mediated through its modulatory influence on hepatic High-Density Lipoprotein (HDL) biogenesis. More recently, Dr. Kabarowski’s group described autoimmune-mediated effects on HDL metabolism in normolipidemic mouse models of Systemic Lupus Erythematosus (SLE) and currently a major effort of his laboratory is directed toward developing therapeutic approaches by which anti-inflammatory and immunosuppressive properties of HDL may be harnessed to improve major Lupus phenotypes and combat premature atherosclerosis, a major cause of morbidity and mortality in this and other rheumatic autoimmune diseases. Emphasis is placed on determining the mechanisms by which protective anti-inflammatory properties of HDL are subverted by chronic inflammation, understanding how this influences immunoregulatory processes involved in SLE and atherosclerosis, and establishing the therapeutic efficacy of HDL-targeted approaches such as HDL mimetic peptides in SLE and other autoimmune diseases.

Selected Publications 
Publication PUBMEDID
Parks BW, Black, LL, Zimmerman, KA, Metz, AE, Steele C, Murphy-Ullrich, JE, Kabarowski JH. CD36, but not G2A, modulates efferocytosis, inflammation and fibrosis following bleomycin-induced lung injury. J Lipid Research. [Epub ahead of print], 2013.   
Tao Yu, Shaohua Yu, Kiran Gupta, Xing Wu, Saman Khaled, Janusz H. Kabarowski, Dennis F. Kucik. Severity of atherosclerosis in ApoE-/- mice following 56Fe irradiation is independent of plasma cholesterol levels. Gra. & Space Biol., 2012.   
Yu T, Parks BW, Yu S, Srivastava R, Gupta K, Wu, X, Khaled S, Chang P, Kabarowski JH, Kucik D. Iron ion (56Fe) radiation increases the size of pre-existing atherosclerotic lesions in ApoE-/- mice. Gravitational and Space Biology. 25(1):57-59, 2011.   
Yu T, Parks BW, Yu S, Srivastava R, Khaled S, Gupta K, Wu, X, Chang P, Kabarowski JH*, Kucik D* (* joint corresponding authors). Iron ion radiation accelerates atherosclerosis in Apolipoprotein-E deficient mice. Radiation Research. 175:766-773, 2011. PMCID: 21466380   
Srivastava, R, Yu, S, Parks, BW, Black, LL, Kabarowski, JH. Autoimmune-mediated reduction of high-density lipoprotein-cholesterol and paraoxonase-1 activity in systemic lupus erythematosus-prone gld mice. Arthritis & Rheumatism. 63:201-211, 2011. PMCID: 3032585   
Parks, BW, Srivastava, R, Yu, S, Kabarowski, JHS. ApoE-dependent modulation of HDL and Atherosclerosis by G2A in LDL receptor-deficient mice independent of bone marrow-derived cells. Arteriosclerosis, Thrombosis and Vascular Biology, 29:539-547, 2009. PMCID: 2679811   
Osmers, I, Parks, BW, Smith, SS, Yu, S, Srivastava, R, Wohler, JE, Barnum, SR, Kabarowski, JHS. Deletion of the G2A receptor fails to attenuate experimental autoimmune encephalomyelitis. J Neuroimmunol, 207:18-23, 2009. PMCID: 2692575   
Parks, BW, Lusis, AJ, Kabarowski, JHS. Loss of the lysophosphatidylcholine effector, G2A, ameliorates aortic atherosclerosis in low-density lipoprotein receptor knockout mice. Arteriosclerosis, Thrombosis and vascular Biology, 26:2703-2709, 2006. PMID: 16990555   
Parks, BW, Gambill, GP, Lusis, AJ, Kabarowski, JHS. Loss of G2A function promotes macrophage accumulation in atherosclerotic lesions of low-density lipoprotein receptor deficient mice. J Lipid Res, 46:1405-1415, 2005. PMID: 15834123   

Keywords
Atherosclerosis, Autoimmunity, HDL, Lipids, Inflammation