Endothelin type B receptor-induced sustained Ca2+ influx involves G(q/11)/phospholipase C-independent, p38 mitogen-activated protein kinase-dependent activation of Na+/H+ exchanger.

Autor: Higa T; Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Sapporo, Japan., Horinouchi T, Aoyagi H, Asano H, Nishiya T, Nishimoto A, Muramatsu I, Miwa S
Jazyk: angličtina
Zdroj: Journal of pharmacological sciences [J Pharmacol Sci] 2010; Vol. 113 (3), pp. 276-80. Date of Electronic Publication: 2010 Jun 29.
DOI: 10.1254/jphs.10102sc
Abstrakt: The mechanism for sustained Ca2+ influx activated by G protein-coupled receptors was examined. In Chinese hamster ovary cells expressing recombinant human endothelin type B receptor (ET(B)R) and endogenous P2Y receptor (P2Y-R), endothelin-1 elicited a sustained Ca2+ influx depending on G(q/11 )protein, phospholipase C (PLC), Na+/H+ exchanger (NHE), and p38 mitogen-activated protein kinase (p38MAPK), whereas P2Y-R-induced sustained Ca2+ influx was negligible. Functional studies showed that NHE activation by ET(B)R was mediated via p38MAPK but not G(q/11)/PLC, while that by P2Y-R involves only G(q/11)/PLC/p38MAPK. These results suggest that G(q/11)/PLC-independent NHE activation via p38MAPK plays an important role in ET(B)R- mediated sustained Ca2+ influx.
Databáze: MEDLINE