CURF 1: Determining the Effect of Protein Prenylation on Retinal Ganglion Cell Death after Acute Retinal Injury

Hello! My name is Jiri Palayekar and I am a freshman at the University of Pittsburgh. As of right now, I have not decided on a major, but I plan to major in either Psychology or Biological Sciences. Something unique about me is that despite my STEM heavy interests, I am quite interested in storytelling and art. I am a part of the Creator’s Collective, which is a student organization on campus where artists, writers, poets, and others gather to discuss what they have been creating and respond to creative challenges at general body meetings. For the Spring semester, I will be working with Dr. Takaaki Kuwajima in his lab for the Chancellor’s Undergraduate Research Fellowship.  

In terms of my current professional goals, I plan on going into medicine. This research project will help me sharpen my skills in analysis and logical thought process and will undoubtedly help me in my future professional goals since medical careers require a lot of deduction-based skill and analysis as well as a familiarity with interpreting research studies and using them to improve patient care. 

Before going to the University of Pittsburgh, I was able to conduct a model organism-based research project focused on the eyesight of fruit flies. Therefore, when I was able to get into a lab which focused on eyes, I was excited because I wanted to expand my interests regarding eye-based research and get more involved in studying the neurological and chemical processes behind eyes.  

90% of all the information used in daily life is visual. Visual information is sent from the eye to the visual centers of the brain via the optic nerve, a bundle of axons emanating from retinal ganglion cells (RGCs).  Damage to the optic nerve after traumatic ocular injuries or in glaucoma inevitably leads to blindness in afflicted patients. Glaucoma affects 64 million people and will take the sight of 111 million people in 2040 in the world [1, 2], and 2.4 million people have ocular injuries in the United States every year. However, there are currently no FDA-approved drugs that maintain the optic nerve integrity and prevent RGC death, and mammalian RGCs lack the ability to regenerate.  

My research, under the guidance of Dr. Kuwajima, will focus on whether treatments with gene therapy, using AAV2-GFP-shFNTA virus which suppresses one of post-translational modifications, protein prenylation protect RGCs and maintain RGC axon connections to the brain in acute ocular disease models such as NMDA excitotoxicity induced RGC death, which is broadly utilized as a model of glaucoma [3-5]. 

1.         Quigley, H.A. and A.T. Broman, The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol, 2006. 90(3): p. 262-7. 

2.         Tham, Y.C., et al., Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology, 2014. 121(11): p. 2081-90. 

3.       Fahrenthold, B.K., K.A. Fernandes, and R.T. Libby, Assessment of intrinsic and extrinsic signaling pathway in excitotoxic retinal ganglion cell death. Sci Rep, 2018. 8(1): p. 4641. 

4.       Christensen, I., et al., The Susceptibility of Retinal Ganglion Cells to Glutamatergic Excitotoxicity Is Type-Specific. Front Neurosci, 2019. 13: p. 219. 

5.       Ullian, E.M., et al., Invulnerability of retinal ganglion cells to NMDA excitotoxicity. MolCell Neurosci, 2004. 26(4): p. 544-57.

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