Pendurthi, Usha, Ph.D.

← BACK  

Contact: usha.pendurthi@uthct.edu

Education:
Ph.D, Biology, 1983, Osmania University , India

Research Interest:

• Blood Coagulation and Fibrinolysis
• Regulation of Gene Expression

Current Projects:

1. Identify the mechanisms by which TF/fVIIa alters cellular processes and influences pathophysiology. Towards this goal, we have identified several potential candidate genes that are upregulated in fibroblasts and cancer cells exposed to fVIIa.
2. Consumption of red wine is believed to provide protection against heart disease. We propose to test the effect of red wine polyphenolic compounds and their analogs on induction of tissue factor and other inflammatory response genes, and assess the effect of these compounds on the development of arteriosclerosis in animal models.

Research Overview:
Blood clotting is a complex biochemical process that impedes blood loss from the traumatized blood vessels and may play a role in healing of the damaged tissues. Circulating blood contains all the soluble clotting precursor factors necessary for blood clotting except ’tissue factor’ (TF). Tissue factor is an integral membrane receptor for soluble factor VII, constitutively expressed in the surrounding tissues of blood vessels. During trauma, circulating factor VII comes in contact with the tissue factor, binds to TF, and subsequently gets activated to enzyme factor VIIa. Tissue factor bound VIIa triggers activation of the coagulation cascade leading to clot formation. Aberrant intravascular expression of tissue factor by a variety of environmental and pathophysiological stimuli could trigger intravascular thrombosis that may result in a heart attack or stroke. Interestingly, several of the enzymes generated during the clotting were also shown to activate cellular signal pathways and to alter their biological function. Thus, clotting enzymes could potentially participate in the physiological process of wound healing and also in pathological processes such as cancer, fibrosis and restenosis. Research in my laboratory focuses on the above area and organized into two projects.

Selected Papers and Abstracts:

• Mandal S, Rao LVM, Tran TT, Pendurthi UR. A novel mechanism of plasmin-induced mitogenesis in fibroblasts. J Thromb Haemost. 2005 Jan;3(1):163-9.
• Mandal S, Iakhiaev A, Pendurthi UR, Rao LV. Acute cholesterol depletion impairs functional expression of tissue factor in fibroblasts. Blood. 2005 Jan 1;105(1):153-60. Epub 2004 Aug 24.
• Rao LVM, Nguyen M, Pendurthi UR. Lethal toxin of Bacillus antracis inhibits tissue factor expression in vascular cells. J Thromb Haemost. 2004 Mar;2(3):530-2.
• Hjortoe GM, Petersen LC, Albrektsen T, Sorensen BB, Norby PL, Mandal S, Pendurthi UR , Rao LVM. Tissue factor-factor VIIa specific up-regulation of IL-8 expression in MDA-MB-231 cells is mediated by PAR-2 and results in increased cell migration. Blood. 2004 Apr 15;103(8):3029-37. Epub 2004 Jan 08.
• Rao LVM, Pendurthi UR. Regulation of tissue factor-factor VIIa expression on cell surfaces: A role for tissue factor- factor VIIa endocytosis. Mol Cell Biochem. 253, 131-140, 2003.
• Pendurthi UR, Rao LVM. Resveratrol suppresses agonist-induced monocyte adhesion to cultured human endothelial cells. Thromb Res. 106 , 243-8, 2002.
• Pendurthi UR, Rao LVM. Effect of wine phenolics and stilbene analogues on tissuefactor expression in endothelial cells. Thromb Res. 106 , 205-11, 2002.
• Shetty S, Pendurthi UR , Halady PK, Azghani AO, Idell S. Urokinase induces its own expression in BEAS-2B lung epithelial cells. Am J Physiol Lung Cell Mol Physiol. 283 , L319-28, 2002.
• Pendurthi UR , Nguyen M, Andrade-Gordon P, Petersen LC, L Rao LV. Plasmin induces Cyr61 gene expression in fibroblasts via protease-activated receptor-1 and p44/42 mitogen-activated protein kinase-dependent signaling pathway. Arterioscler Thromb Vasc Biol. 22 , 1421-6, 2002.
• Samten B, Ghosh P, Yi AK, Weis SE, Lakey DL, Gonsky R, Pendurthi U , Weisel B, Zhang Y, Zhang M, Gong J, Fernandez M, Safi H, Vankayalapati R, Young HA, and Barnes PF. Reduced expression of nuclear cyclic adenosine 5’-monophosphate response element-binding proteins and IFN-gamma promoter function in disease due to and intracellular pathogen. J Immunol 168 , 3520-6, 2002.