Associate Professor of Ophthalmology, Pharmacology and Cancer Biology

Education

Osmania University, PhD in Biochemistry

Phone

919-681-5883

Email

rao00011@mc.duke.edu

Research Interests

Research in Rao's laboratory focuses on two areas of ocular diseases cataract and glaucoma. As it relates to glaucoma, his research is focused to elucidate intracellular signaling pathways regulating aqueous humor outflow facility through trabecular meshwork. Identifying potential regulatory mechanisms controlling aqueous humor outflow resistance has important implications for understanding glaucoma and developing effective therapies to lower intraocular pressure. Recent work from this laboratory, based on pharmacological and genetic manipulation of Rho/Rho kinase pathway, strongly suggested that Rho kinase is a potential target for therapeutic modulation of outflow facility in glaucoma patients. Rao's approaches include molecular, physiological and pharmacological using primary cell cultures of human trabecular meshwork, Schlemm’s canal and ciliary muscle tissues and porcine or human whole eyes. His ongoing research is focused on understanding the regulation of myosin II phosphorylation, contractile properties and extracellular matrix production and turnover of trabecular meshwork and ciliary body cells. 

Research as it relates to cataract and lens biology, his primary goal is to identify and characterize the critical signaling mechanisms involved in the regulation of lens fiber cell elongation and differentiation and understand their potential role in cataractogenisis. His recent work, based on the development of a transgenic lens specific functional knockout of Rho GTPase and over expression of Rho GDI in transgenic mouse lens revealed that Rho GTPases play an essential role in regulating lens growth and development, and that their inactivation leads to abnormal lens growth and development in the mouse model. His ongoing work is focused on elucidating the mechanistic roles of Rho and Rac GTPases in lens growth factor signaling, and in lens fiber cell elongation and differentiation. 

The long-term goals of his laboratory are to provide potential therapeutic avenues for drug development to treat glaucoma and cataract.

Representative Publications

1. Zhang M, Rao PV. Blebbistatin, a Novel Inhibitor of Myosin II ATPase Activity Increases Aqueous Humor Outflow Facility in Perfused Enucleated Porcine Eyes. Invest. Ophthalmol. Vis. Sci. IOVS 2005, in press.
2. Song J, Stinnett SS, Deng P, Epstein DL, P. V. Rao. Effects of Cholesterol Lowering Statin Drugs on the Aqueous Humor Outflow Pathway. Invest. Ophthalmol. Vis. Sci. 2005; 46, 2424-2432.
3. Maddala R, Rao, P.V. AlphaB-crystallin localizes to the leading edges of migrating lens epithelial cells. Exp Cell Res. 2005; 306, 203-215.
4. Rao PV, Deng PF, Maddala R, Epstein DL, Li, CH, Shimokawa H. Expression of Dominant Negative Rho-Binding Domain of Rho-Kinase in Organ Cultured Human Eye Anterior Segments Increases Aqueous Humor Outflow. Mol. Vision. 2005; 11: 288-297.
5. Mettu PS, Deng P, Misra U, Epstein DL, Rao PV. Role of Lysophospholipid Growth Factors and Edg Receptors in the Modulation of Aqueous Humor Outflow Facility. Invest. Ophthalmol. Vis. Sci. 2004; 45: 2263-2271.
6. Maddala R, ReddyVN, Epstein DL, Rao PV. Growth Factor-Induced activation of Rho and Rac GTPases and Actin Cytoskeletal Reorganization in Human Lens Epithelial Cells. Mol. Vision. 2003; 9: 329-336.
7. Rao PV, Wawrousek E, Tamm ER, Zigler Jr. Rho GTPase inactivation impairs lens growth and integrity. Lab. Invest. 2002; 82: 231-239. 
8. Rao PV, Deng PF, Kumar J, Epstein DL. Modulation of aqueous humor outflow facility by the Rho kinase specific inhibitor Y-27632. Invest. Ophthalmol. Vis. Sci. 2001; 42: 1029-1037.
9. Maddala RL, Peng YW, Rao PV. Selective expression of the small GTPase RhoB in the early developing mouse lens. Devel. Dyn. 2001; 222: 534-537.
10. Rao PV, Allingham RR, Epstein DL. TIGR/Myocilin in human aqueous humor. Exp. Eye Res. 2000; 71: 637-641.