Honors Theses

Date of Award

Spring 4-30-2021

Document Type

Undergraduate Thesis

Department

Chemistry and Biochemistry

First Advisor

Jason Paris

Second Advisor

Nicole Ashpole

Third Advisor

Saumen Chakraborty

Relational Format

Dissertation/Thesis

Abstract

Great advances have been made in the treatment of HIV, however, new infections remain consistent each year with no effective cure. The early entry of HIV virus into the central nervous system is thought to contribute to the development of HIV-associated neurocognitive disorders. One of the mechanisms of neurological impairment may involve actions of the neurotoxic HIV viral protein, trans-activator of transcription (Tat). Tat can be secreted from infected cells and acts as an excitotoxin, increasing the intracellular flux of Ca2+ , promoting mitochondrial dysfunction, and neural cell damage/death. Previous experiments have shown that steroid hormones such as estrogen can exert protective effects against Tat-mediated neurotoxicity; but, the site(s) of this protection action are unclear. The primary purpose of this thesis was to begin to assess the role of the non-traditional estrogen receptor, G-protein coupled receptor 1 (GPER1), in Tat-mediated neurotoxicity. The capacity of a GPER1 agonist and antagonist were assessed for their influence on Tat-induced production of reactive oxygen species (ROS) and subsequent cell death using SH-SY5Y human neuroblastoma cells. The results revealed that GPER1 agonism attenuated Tat induced ROS production and prevented Tat-mediated cell death. Conversely, antagonizing GPER1 modestly reduced ROS production; albeit, did not completely attenuate Tat-mediated increases, and exert no effects on cell death. Further investigation of non-traditional sites of endocrine action may reveal novel therapeutic targets for the treatment of neurological diseases, within and beyond the field of neuroHIV.

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