Involvement of P38 Mapk in Hypotonic Stress-induced Stimulation of Beta- and Gamma-enac Expression in Renal Epithelium.
From: Department of Molecular Cell Physiology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Biochemical and biophysical research communications
- Publish Date: Jul 2007
- ISSN: 0006-291X
- Volume: 358
- Issue: 3
- Pages: 819-24
- Medium: Print
- Language: English
- Citation (JAMA): Niisato Naomi, Taruno Akiyuki, Marunaka Yoshinori, et al. Involvement of P38 Mapk in Hypotonic Stress-induced Stimulation of Beta- and Gamma-enac Expression in Renal Epithelium.. Biochem. Biophys. Res. Commun. Jul 2007;358:819-24
Abstract
We investigated a role of p38 MAPK in the regulation of transepithelial Na(+) reabsorption by chronic application (20-24h) of hypotonicity (hypotonic stress) in renal epithelial A6 cells. Pretreatment with a specific p38 MAPK inhibitor (SB202190) significantly reduced the chronic hypotonicity-stimulated transepithelial Na(+) reabsorption by diminishing the Na(+) entry through epithelial Na(+) channel (ENaC) in the apical membrane and the Na(+) extrusion via the Na(+)/K(+) ATPase (pump), although the rate limiting step was still the Na(+) entry step. We further examined whether the inhibitory effects of SB202190 on the transepithelial Na(+) reabsorption is caused through suppression of mRNA expression of ENaC participating in the transepithelial Na(+) reabsorption as the Na(+) entry pathway. The chronic hypotonicity increased the mRNA expression of alpha-, beta-, and gamma-subunits of ENaC. Moreover, we found that inhibition of p38 MAPK by SB202190 diminished the mRNA expression of beta- and gamma-ENaC but not alpha-ENaC. Based on these observations, it is suggested that the chronic hypotonicity stimulates the renal transepithelial Na(+) reabsorption by upregulating the mRNA expression of beta- and gamma-ENaC via a p38 MAPK-dependent pathway.
Mesh Headings (Keywords): Animals, Electrophysiology, Enzyme Inhibitors, Epithelial Sodium Channel, Epithelium, Gene Expression Regulation, Imidazoles, Kidney, Pyridines, RNA, Messenger, Sodium Channels, Sodium-Potassium-Exchanging ATPase, Stress, Up-Regulation, Xenopus laevis, p38 Mitogen-Activated Protein Kinases
Check for Full Text / PubMed Unique Identifier (PMID): 17506993
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.