Department of Ophthalmology

Shahid Husain, Ph.D.

Photo of Dr. Husain



ABBREVIATED CV OF Dr. Husain

PEER-REVIEWED PUBLICATIONS 2009-2014

GRANT SUPPORT 2009-2014

PICTURES OF LABORATORY ACTIVITIES

LABORATORY PERSONNEL
 
Principal Investigator, Shahid Husain, Ph.D.
  Postdoctoral Scholar, Yasir Abdul, Ph.D.
  Postdoctoral Scholar, Naseem Akhter, Ph.D.
  Research Tech I, Melissa Nix, B.S.
  Research Tech I, Sudha Singh, B.S.












SUMMARY OF LABORATORY RESEARCH GOALS
Primary goals of my research are to investigate the signaling mechanisms that are involved in ischemia- and glaucoma-induced optic nerve damage and retina ganglion cell death using various in vivo and culture models.  A variety of neuroprotective agents have been applied in these models to assess their efficacy and effectiveness to protect optic nerve and retinal ganglion cells against ischemic and glaucomatous injury.  In addition, my laboratory is actively engaged in evaluating signaling mechanisms that are involved in the lowering of intraocular pressure in normal and hypertensive models.  The long-term goals of my research projects are:

1. To identify factors that are responsible for optic nerve and retinal ganglion cells degeneration in ischemia and glaucoma and to develop neuroprotective strategies that delay (or prevent) vision loss in glaucoma.

2.  To understand that how the catabolic (e.g., prostaglandins, adenosine, and pro-inflammatory cytokines), and anti-catabolic (e.g., glucocorticoids and anti-inflammatory cytokines) regulators influence aqueous humor dynamics and the expression/activation of matrix metalloproteinases (MMPs) and their inhibitors from human ciliary muscle and trabecular meshwork cells.

OVERVIEW

Glaucoma, one of the world’s leading causes of visual impairment and blindness, is characterized by excavation of the optic nerve head and selective apoptotic loss of retinal ganglion cells (RGCs), resulting in a progressive decline in visual function.  Nearly 67 million people worldwide are believed to have glaucoma, including an estimated 2.2 million in the USA.  The etiology of optic neuropathy is complex involving metabolic and biomechanical stress to the optic nerve head.  The activation of astrocytes appears to play a central role in progressive optic neuropathy, serving as the cellular source of multifunctional cytokines and enzymes (e.g., MMPs) responsible for remodeling the extracellular matrix within the optic nerve head.

In mammals, endogenous opioidergic peptides, such as enkephalins, dynorphins, and endorphins, are physiological modulators of neuroendocrine, immune, and inflammatory challenges that are released in response to stress.  The effects of opioids are mediated through activation of three, opioid receptor subtypes (d, k, and m).  Under stressful conditions (e.g., ischemic, oxidative, and inflammatory stress), endogenous opioidergic peptides are released reducing stress-related injuries.  In addition, activation of opioid-receptors by an exogenous agonist has been shown to elicit a protective effect during situations of stress.  A clear understanding of the roles of opioid-receptor subtypes and the cellular events involved in opioid-agonist-evoked neuroprotection in the retina and optic nerve head are not only innovative, but they will provide valuable leads for the discovery of more effective therapies that can delay or prevent vision loss associated with glaucoma.

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