GADIPARTHI N. RAO, Ph.D.

Professor

Office: 310J TRANSLATIONAL RESEARCH BUILDING
71 SOUTH MANASSAS
MEMPHIS TN 38163
Tel: (901) 448-7321
rgadipar@uthsc.edu

Research description

Increased arterial smooth muscle cell growth and accumulation of extracellular matrix proteins are associated with the development of these vascular lesions. We believe that a change in the redox state of the arterial wall triggers these pathological events. Therefore, the major interest of our laboratory is to study the regulation and signal transduction mechanisms of redox-sensitive gene expression in vessel wall cells and investigate their role in atherosclerosis and neointima formation using animal models. The major techniques used in the laboratory are rat carotid artery injury, Northern blot analysis, Western blot analysis, nuclear run-on assay, electrophoretic mobility shift assay, 2-D gel electrophoresis, high performance liquid chromatography, tube formation assay, cell migration assay, tissue culture, transfections, immunohistochemistry, Matrigel plug angiogenesis, chromatin immunoprecipitation assay, RT-PCR and molecular cloning.

Research interest/specialty

Atherosclerosis and restenosis after angioplasty are the major cardiovascular problems particularly in western countries.

Research keywords

Atherosclerosis, restenosis, angioplasty, RT-PCR, molecular cloning.

Research interest/specialty

Atherosclerosis and restenosis after angioplasty are the major cardiovascular problems particularly in western countries.

Research keywords

Atherosclerosis, restenosis, angioplasty, RT-PCR, molecular cloning.

Research description

Increased arterial smooth muscle cell growth and accumulation of extracellular matrix proteins are associated with the development of these vascular lesions. We believe that a change in the redox state of the arterial wall triggers these pathological events. Therefore, the major interest of our laboratory is to study the regulation and signal transduction mechanisms of redox-sensitive gene expression in vessel wall cells and investigate their role in atherosclerosis and neointima formation using animal models. The major techniques used in the laboratory are rat carotid artery injury, Northern blot analysis, Western blot analysis, nuclear run-on assay, electrophoretic mobility shift assay, 2-D gel electrophoresis, high performance liquid chromatography, tube formation assay, cell migration assay, tissue culture, transfections, immunohistochemistry, Matrigel plug angiogenesis, chromatin immunoprecipitation assay, RT-PCR and molecular cloning.

Publications

  1. Cheranov, SY, Karpurapu, M, Wang, D, Zhang, B, Venema, RC, Rao, GN. An essential role for SRC-activated STAT-3 in 14,15-EET-induced VEGF expression and angiogenesis. Blood, 111 (12), 5581-91, 2008.
  2. Bajpai, AK, Blaskova, E, Pakala, SB, Zhao, T, Glasgow, WC, Penn, JS, Johnson, DA, Rao, GN. 15(S)-HETE production in human retinal microvascular endothelial cells by hypoxia: Novel role for MEK1 in 15(S)-HETE induced angiogenesis. Invest Ophthalmol Vis Sci, 48 (11), 4930-8, 2007.
  3. Kundumani-Sridharan, V, Wang, D, Karpurapu, M, Liu, Z, Zhang, C, Dronadula, N, Rao, GN. Suppression of activation of signal transducer and activator of transcription-5B signaling in the vessel wall reduces balloon injury-induced neointima formation. Am J Pathol, 171 (4), 1381-94, 2007.
  4. Srivastava, K, Kundumani-Sridharan, V, Zhang, B, Bajpai, AK, Rao, GN. 15(S)-hydroxyeicosatetraenoic acid-induced angiogenesis requires STAT3-dependent expression of VEGF. Cancer Res, 67 (9), 4328-36, 2007.
  5. Wang, D, Liu, Z, Li, Q, Karpurapu, M, Kundumani-Sridharan, V, Cao, H, Dronadula, N, Rizvi, F, Bajpai, AK, Zhang, C, Müller-Newen, G, Harris, KW, Rao, GN. An essential role for gp130 in neointima formation following arterial injury. Circ Res, 100 (6), 807-16, 2007.
  6. Cao, H, Dronadula, N, Rizvi, F, Li, Q, Srivastava, K, Gerthoffer, WT, Rao, GN. Novel role for STAT-5B in the regulation of Hsp27-FGF-2 axis facilitating thrombin-induced vascular smooth muscle cell growth and motility. Circ Res, 98 (7), 913-22, 2006.
  7. Dronadula, N, Rizvi, F, Blaskova, E, Li, Q, Rao, GN. Involvement of cAMP-response element binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility. J Lipid Res, 47 (4), 767-77, 2006.
  8. Zhang, B, Cao, H, Rao, GN. Fibroblast growth factor-2 is a downstream mediator of phosphatidylinositol 3-kinase-Akt signaling in 14,15-epoxyeicosatrienoic acid-induced angiogenesis. J Biol Chem, 281 (2), 905-14, 2006.
  9. Cao, H, Dronadula, N, Rao, GN. Thrombin induces expression of FGF-2 via activation of PI3K-Akt-Fra-1 signaling axis leading to DNA synthesis and motility in vascular smooth muscle cells. Am J Physiol Cell Physiol, 290 (1), C172-82, 2006.
  10. Zhang, B, Cao, H, Rao, GN. 15(S)-hydroxyeicosatetraenoic acid induces angiogenesis via activation of PI3K-Akt-mTOR-S6K1 signaling. Cancer Res, 65 (16), 7283-91, 2005.
  11. Liu, Z, Zhang, C, Dronadula, N, Li, Q, Rao, GN. Blockade of nuclear factor of activated T cells activation signaling suppresses balloon injury-induced neointima formation in a rat carotid artery model. J Biol Chem, 280 (15), 14700-8, 2005.
  12. Dronadula, N, Liu, Z, Wang, C, Cao, H, Rao, GN. STAT-3-dependent cytosolic phospholipase A2 expression is required for thrombin-induced vascular smooth muscle cell motility. J Biol Chem, 280 (4), 3112-20, 2005.
  13. Neeli, I, Liu, Z, Dronadula, N, Ma, ZA, Rao, GN. An essential role of the Jak-2/STAT-3/cytosolic phospholipase A(2) axis in platelet-derived growth factor BB-induced vascular smooth muscle cell motility. J Biol Chem, 279 (44), 46122-8, 2004.
  14. Liu, Z, Dronadula, N, Rao, GN. A novel role for nuclear factor of activated T cells in receptor tyrosine kinase and G protein-coupled receptor agonist-induced vascular smooth muscle cell motility. J Biol Chem, 279 (39), 41218-26, 2004.
  15. Zhuang, D, Ceacareanu, AC, Lin, Y, Ceacareanu, B, Dixit, M, Chapman, KE, Waters, CM, Rao, GN, Hassid, A. Nitric oxide attenuates insulin- or IGF-I-stimulated aortic smooth muscle cell motility by decreasing H2O2 levels: essential role of cGMP. Am J Physiol Heart Circ Physiol, 286 (6), H2103-12, 2004.
  16. Neeli, I, Yellaturu, CR, Rao, GN. Arachidonic acid activation of translation initiation signaling in vascular smooth muscle cells. Biochem Biophys Res Commun, 309 (4), 755-61, 2003.
  17. Yellaturu, CR, Rao, GN. A requirement for calcium-independent phospholipase A2 in thrombin-induced arachidonic acid release and growth in vascular smooth muscle cells. J Biol Chem, 278 (44), 43831-7, 2003.
  18. Yellaturu, CR, Rao, GN. Cytosolic phospholipase A2 is an effector of Jak/STAT signaling and is involved in platelet-derived growth factor BB-induced growth in vascular smooth muscle cells. J Biol Chem, 278 (11), 9986-92, 2003.
  19. Bhanoori, M, Yellaturu, CR, Ghosh, SK, Hassid, A, Jennings, LK, Rao, GN. Thiol alkylation inhibits the mitogenic effects of platelet-derived growth factor and renders it proapoptotic via activation of STATs and p53 and induction of expression of caspase1 and p21(waf1/cip1). Oncogene, 22 (1), 117-30, 2003.
  20. Yellaturu, CR, Ghosh, SK, Rao, RK, Jennings, LK, Hassid, A, Rao, GN. A potential role for nuclear factor of activated T-cells in receptor tyrosine kinase and G-protein-coupled receptor agonist-induced cell proliferation. Biochem J, 368 (Pt 1), 183-90, 2002.
  21. Zeng, ZZ, Yellaturu, CR, Neeli, I, Rao, GN. 5(S)-hydroxyeicosatetraenoic acid stimulates DNA synthesis in human microvascular endothelial cells via activation of Jak/STAT and phosphatidylinositol 3-kinase/Akt signaling, leading to induction of expression of basic fibroblast growth factor 2. J Biol Chem, 277 (43), 41213-9, 2002.
  22. Yellaturu, CR, Bhanoori, M, Neeli, I, Rao, GN. N-Ethylmaleimide inhibits platelet-derived growth factor BB-stimulated Akt phosphorylation via activation of protein phosphatase 2A. J Biol Chem, 277 (42), 40148-55, 2002.
  23. Ghosh, SK, Gadiparthi, L, Zeng, ZZ, Bhanoori, M, Tellez, C, Bar-Eli, M, Rao, GN. ATF-1 mediates protease-activated receptor-1 but not receptor tyrosine kinase-induced DNA synthesis in vascular smooth muscle cells. J Biol Chem, 277 (24), 21325-31, 2002.