Shravan K. Chintala
Biography
Dr. Shravan K. Chintala received a Ph.D. in microbiology from Osmania University in India in 1992. He obtained his formal training in cell biology at Cleveland Clinic Foundation (1992-95) and molecular biology and neuroscience at UT M.D. Anderson Cancer Center (1995-1999).
Chintala has extensive experience on small animal models related to glaucoma and on the function of matrix metalloproteinases (MMPs) and plasminogen activators in the death of retinal ganglion cells. He is one of the team members who has identified ELAM-1 (endothelial leukocyte adhesion molecule) as the first known molecular marker for glaucoma in humans. Chintala previously received funding from the Massachusetts Lions Eye Research Fund and the National Eye Institute.
Research
Chintala’s laboratory research is focused on the role of proteases in the death of retinal ganglion cells (RGCs) in glaucoma.
Primary open-angle glaucoma (POAG) is the second leading cause of blindness, which affects more than 60 million people worldwide. POAG is a multi-factorial neurodegenerative disease, characterized by the progressive and irreversible loss of RGCs and their axons. Although an elevation in intraocular pressure (IOP) remains the only proven risk factor, the mechanisms that initiate the insult and subsequently lead to the death of RGC death in POAG are poorly understood. Chintala is elucidating whether elevated levels of matrix metalloproteinase-9 (MMP-9), tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA) degrades the extracellular matrix (ECM) in the ganglion cell layer, and the degradation of ECM then leads to the death of retinal ganglion cells. The long-term goal of his laboratory is to develop pharmacological agents that inhibit the action of these proteases and to prevent ganglion cell loss in glaucoma.
Select Publications: (see https://sites.google.com/a/oakland.edu/chintala/ for complete list)
Wang, N., Chintala, S.K., Fini, M. E., and Schuman, J.S. Activation of a tissue-specific response in the eye’s aqueous outflow pathway defines glaucoma disease phenotype. Nature Medicine, (2001), 7(6): 304-309.
Chintala, S.K., Zhang, Xu., Austin, J.F., Fini, M.E. Deficiency in Matrix Metalloproteinase Gelatinase B (MMP-9) Protects against Retinal Ganglion Cell Death after Optic Nerve Ligation. Journal of Biological Chemistry, (2002), 277: 47461-47468.
Zhang, X., Chaudhry, A., and Chintala, S.K. Inhibition of plasminogen activation protects against ganglion cell loss in a mouse model of optic nerve damage. Molecular Vision, (2003), 9: 238-248
Zhang, X., and Chintala, S.K. Glial Cells Contribute to Matrix Metalloproteinase-9 Induction in the retina following optic nerve ligation. Neuroscience Letters, (2004), 356, 140-144.
Zhang, X., and Chintala, S.K. Influence of Interleukin-1beta and mitogen-activated protein kinase phosphorylation on optic nerve ligation-induced matrix metalloproteinase-9 induction in the retina. Experimental Eye Research, (2004), 78, 849-860.
Zhang, X., Cheng, M., and Chintala, S.K. Kainic acid-mediated upregulation of matrix metalloproteinase-9 promotes retinal degeneration. Investigative Ophthalmology & Vision Science, (2004), 45: 2374-2383.
Mali, R.S., Cheng, M., and Chintala, S.K. Intravitreous injection of membrane depolarization agent causes retinal degeneration via Matrix Metalloproteinase-9. Investigative Ophthalmology & Vision Science, (2005), 46: 2125-2132.
Mali, R.S., Cheng, M., and Chintala, S.K. Plasminogen activators promote excitotoxicity-induced retinal degeneration. FASEB J, (2005), 19: 1280-1289.
Chintala, S.K. The emerging role of proteases in retinal ganglion cell death. Experimental Eye Research, (2006), 82: 5-12.