Janusz H.S. Kabarowski, PhD
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.
Lipids and lipoprotein metabolism in chronic inflammatory disease
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.
- Black LL, Srivastava R, Schoeb TR, Moore RD, Barnes S, Kabarowski JH..
Cholesterol-Independent Suppression of Lymphocyte Activation, Autoimmunity, and Glomerulonephritis by Apolipoprotein A-I in Normocholesterolemic Lupus-Prone Mice.
J Immunol. 2015 Nov 15;195(10):4685-98. doi: 10.4049/jimmunol.1500806. Epub 2015 Oct 14. [PMID: 26466956]
- Lopez EL, Kabarowski JH, Ingle KA, Kain V, Barnes S, Crossman D, Lindsey ML, Halade GV.
Obesity superimposed on aging magnifies inflammation and delays the resolving response after myocardial infarction.
Am J Physiol Heart Circ Physiol. 2015 Feb 15;308(4):H269-80. [doi: 10.1152/ajpheart.00604.2014] Epub 2014 Dec 5. [PMID: 25485899]
- 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 Res. 2013 Apr;54(4):1114-23. doi: 10.1194/jlr.M035352. Epub 2013 Feb 6. [PMID: 23393303]
- 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