Shahid Husain, PhD
My primary research focus is to develop neuroprotective strategies and agents for the treatment of glaucoma and ischemia/reperfusion-induced retinopathies. An emerging hypothesis suggests that a) an hypoxic component in response to glaucomatous injury plays key role in the degeneration of retinal ganglion cells (RGC), and b) that the blockage of hypoxia-inducible transcription factor-1α (HIF-1α) activity/expression can rescue RGCs. Elevated levels of HIF-1α in human glaucoma and experimental glaucoma models have been shown. However, the molecular mechanisms involved in HIF-1α-induced RGC death are not clearly defined. I have the necessary expertise, leadership, training, and motivation to carry out this research project, including a strong background in ocular pharmacology, physiology, electrophysiology, immunology, signal transduction, and protein biochemistry. I was trained as a protein biochemist during my doctoral work, then completed postdoctoral training in ocular pharmacology studying therapeutic potentials of numerous intraocular pressure-lowering drugs and their impact on aqueous humor dynamics. I have extensive experience in signal transduction work (e.g., cAMP, Ca+2, protein kinases and phosphatases) using ocular and non-ocular tissues. During the last decade, my laboratory has been working to define neurodegeneration mechanisms in glaucoma and ischemia/reperfusion-related retinopathies using a variety of techniques (including immunological techniques) and agents. My laboratory has identified several molecules and ligands that can provide retina neuroprotection against glaucoma and ischemia/reperfusion-induced retinal injuries as determined by various in vitro (e.g., RGCs, ONH astrocytes, microglia cells) and in vivo (Morrison and microbead glaucoma models, and acute ischemia model) approaches.