Angii-mediated Regulation of Beta-Arrestins Expression in Spontaneously hypertensive Rat (SHR) and Wistar Rat Astrocytes

POSTER PRESENTATIONS

Objective. Study the effect of angiotensine II (AngII) on the expression level of beta-arrestins in astrocytes isolated from the brainstem of SHR and Wistar rats. Background. The beta-arrestins (beta-arrestin1 and-2) originally discovered as terminators of G protein signaling by G protein-coupled receptors (GPCRs) are now known to also mediate their own signaling independently of G proteins. Little is known about the cellular distribution and regulation of beta-arrestins protein and gene expression in brain tissues. Methods. Primary cultures of brainstem astrocytes were isolated from the brains of 2-3 days old SHR and Wistar rat pups. To test the effect of AngII on the protein and mRNA levels of beta-arrestin1 and-2, primary astrocytes were treated with 100 nM AngII at different time points. Protein analysis was done using Western blotting technique and mRNA measurement was done using real time PCR technique. Results. Our results showed that beta-arrestin1 is the major arrestin protein in astrocytes in both SHR and Wistar rats. But at the mRNA level both beta-arrestin1 and-2 have comparable expressions. AngII upregulates beta-arrestin1 protein in Wistar rats, while in SHR AngII had no significant effect on protein expression. AngII down regulates both beta-arrestin1 and-2 mRNA expressions in both models. Conclusion. In this study, we showed that beta-arrestin1 is expressed in brainstem astrocytes and that its level are responsive to AngII. Further, our studies suggest that beta-arrestin1 protein expression maybe impaired in the hypertensive model and possibly may play a role in high blood pressure observed in this model. Grants. Funding for this research was provided through a Nova Southeastern University Health Professions Division Grant.