RGS2 regulates urotensin II-induced intracellular Ca2+ elevation and contraction in glomerular mesangial cells.

ABSTRACT: Urotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular mesangial cells (GMCs). This study also tested the hypothesis that the regulator of G-protein signaling (RGS) controls UII receptor (UTR) activity in GMCs. RT-PCR, Western immunoblotting, and immunofluorescence revealed UTR expression in cultured murine GMCs. Mouse UII (mUII) stimulated Ca(2+) release from intracellular stores and activated store-operated Ca(2+) entry (SOCE) in the cells. mUII also caused a reduction in planar GMC surface area. mUII-induced [Ca(2+)]i elevation and contraction we

SUBMITTER: Adebiyi A 

PROVIDER: S-EPMC11250777 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature