Mark B. Taubman, M.D.
|Dean, School of Medicine & Dentistry - Department of Dean's Office, SMD
|CEO, University of Rochester Medical Center - Department of Office of VP for Health Sciences (URMC)|
|Professor - Department of Medicine, Cardiology|
|1978 | MD | Medicine | New York Univ Sch Medicine|
|1976 | MS | Pre-Medical | New York Univ Sch Medicine|
|1972 | BA | Biochemistry | Columbia University|
Dr. Taubman's laboratory is focused on the role of vascular smooth muscle cells (SMC) in regulating inflammation and thrombosis in the arterial wall.
There are three major areas of investigation:
- Tissue factor, the initiator of coagulation, is highly regulated by growth factors in SMC and is induced in the arterial wall after balloon injury. Ongoing studies involve the regulation of tissue factor expression in SMC culture and the regulation of tissue factor expression and activity in the injured vessel wall and in animal models of atherosclerosis. Recent data has shown that tissue factor can be released from the cell wall in microparticles and that these particles retain the ability to activate coagulation. In addition, there is an alternatively spliced form of tissue factor that is soluble and circulates in the blood. We are trying to understand the role of these forms of circulating tissue factor in mediating arterial thrombosis using mice with tissue-specific tissue factor deletions and mice expressing only full-length or alternative-spliced forms of tissue factor.
- MCP-1 encodes a monocyte chemoattractant that, like tissue factor, is regulated by growth factors in SMC culture and in the vessel wall after balloon injury. Ongoing studies involve examination of MCP-1 regulation in cell culture and in animal models of arterial disease. A particular focus has been the regulation of MCP-1 mRNA stability by PDGF and glucocorticoids. Studies are focused on identifying the proteins and signaling pathways that regulate MCP-1 mRNA stability. Such studies may provide novel approaches to attenuate the inflammatory process.
- EGLN3/SM-20 encodes an intracellular prolyl hydroxylase that regulates the response of cells to hypoxia. We have recently determined that EGLN3 also plays a key role in muscle cell differentiation and are currently exploring the mechanism underlying this finding. Studies are ongoing to elucidate the function of this gene using muscle cell cultures and by generating an EGLN3 knockout mouse. EGLN3 is also being analyzed using in vitro and in vivo models to examine its regulation in response to ischemia.
- Vascular effects of ultrafine particles in persons with type 2 diabetes.
Stewart JC, Chalupa DC, Devlin RB, Frasier LM, Huang LS, Little EL, Lee SM, Phipps RP, Pietropaoli AP, Taubman MB, Utell MJ, Frampton MW.
Environ Health Perspect. 2010 Dec;118(12):1692-8. Epub 2010 Sep 7.
- Protein kinase Cδ mediates MCP-1 mRNA stabilization in vascular smooth muscle cells. Liu B, Dhawan L, Blaxall BC, Taubman MB.
Mol Cell Biochem. 2010 Nov;344(1-2):73-9. Epub 2010 Jul 4.
- Prolyl hydroxylase EGLN3 regulates skeletal myoblast differentiation through an NF-kappaB-dependent pathway. Fu J, Taubman MB.
J Biol Chem. 2010 Mar 19;285(12):8927-35. Epub 2010 Jan 10.
- Platelets and megakaryocytes contain functional nuclear factor-kappaB.
Spinelli SL, Casey AE, Pollock SJ, Gertz JM, McMillan DH, Narasipura SD, Mody NA, King MR, Maggirwar SB, Francis CW, Taubman MB, Blumberg N, Phipps RP. Arterioscler Thromb Vasc Biol. 2010 Mar;30(3):591-8. Epub 2009 Dec 30.
- Role of tissue factor in cancer. Kasthuri RS, Taubman MB, Mackman N.
J Clin Oncol. 2009 Oct 10;27(29):4834-8. Epub 2009 Sep 8. Review.
Mark B. Taubman , M.D.
University of Rochester
601 Elmwood Ave, Box 706
Rochester, New York 14642
Admin. Office: (585) 276-9800
Research Assistant Professor
Research Assistant Professor