Â鶹´«Ã½Ó³»­

Â鶹´«Ã½Ó³»­

Explore the latest content from across our publications
Join The Â鶹´«Ã½Ó³»­

Log In

Forgot Password?
Create New Account

Loading... please wait

Abstract Details

The Effect of Sex Hormones on the Secretion of the Insulin Receptor in HIV Infection
Infectious Disease
P11 - Poster Session 11 (8:00 AM-9:00 AM)
13-001
To determine if testosterone and beta-estradiol exposure in differentiated neuroblastoma cell cultures confers any protective effect against Tat-mediated neurotoxicity, and if Tat is indirectly affecting the neuroprotective role of beta-estradiol.
HIV-1 infection may result in development of HIV-associated neurocognitive disorders (HAND). Although its pathogenesis is not clearly understood, it is known that the HIV-regulatory protein Tat is released from infected cells and is implicated in mediating neuronal dysfunction. Furthermore, levels of the soluble insulin receptor (sIR) levels have been shown to be positively associated with the degree of HAND progression. 
SH-SY5Y neuroblastoma cell line was cultured, differentiated, and treated with different combinations of the viral protein Tat, beta-estradiol, testosterone, and inhibitors of sex hormone receptors. Insulin receptor ELISA was then performed on supernatants to measure sIR secretion as a measure of neurotoxicity. Human estrogen receptor beta (ER) was then immunoprecipitated from cell extracts in an attempt to co-immunoprecipitate Tat protein.
Treatment with sex hormones and Tat, independently have the effect of inducing more sIR release. However, when both treatments are coupled, they showed no effect in sIR secretion. Moreover, estradiol was not neuroprotective as expected. We hypothesized that this paradoxical results would be mediated by an interaction between Tat protein and the estrogen receptor. However our co-immunoprecipitation results showed no interactions between these two proteins. 
Despite independently causing an increase in sIR secretion, when combined, Tat and sex hormone treatments showed no effect. This phenomenon can not be explained by a Tat-ER protein interaction. More experiments are needed to determine if HIV-Tat is indirectly affecting the neuroprotective role of beta estradiol in neurons specifically.
Authors/Disclosures
Miguel A. Santiago-Cruz (UIC Neurology & Rehabilitation, MC 796)
PRESENTER 		No disclosure on file
Rafael Brito No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
Valerie E. Wojna, MD, FÂ鶹´«Ã½Ó³»­ (Nuerology Division, UPR MSC SoM) Dr. Wojna has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Puerto Rico Health Sciences Journal, University of Puerto Rico Medical Sciences Campus. The institution of Dr. Wojna has received research support from NIH.