Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

ENaC proteins contribute to VSMC migration.

Authors: Grifoni, SC  Gannon, KP  Stec, DE  Drummond, HA 
Citation: Grifoni SC, etal., Am J Physiol Heart Circ Physiol. 2006 Dec;291(6):H3076-86. Epub 2006 Jul 14.
Pubmed: (View Article at PubMed) PMID:16844921
DOI: Full-text: DOI:10.1152/ajpheart.00333.2006

Vascular smooth muscle cell (VSMC) migration plays a key role in tissue repair after arterial wall injury. VSMC migration requires integration of chemical and mechanical signaling mechanisms. Recently, we showed that epithelial Na(+) channel (ENaC) proteins are expressed in VSMCs and that ENaC inhibition abolishes pressure-induced constriction in isolated artery segments. However, whether ENaC proteins play a role in VSMC migration is unknown. The goal of this study was to determine whether ENaC molecules are required for VSMC migration. Using RT-PCR, immunoblotting, and immunolabeling, we detected expression of alpha-, beta-, and gammaENaC transcripts and proteins in cultured VSMCs (SV40-LT and A10 cells). Of the three proteins, betaENaC was the most readily detected in both cell lines by immunolocalization and Western blotting. Inhibition of ENaC activity with 1 microM benzamil blunted VSMC migration associated with wound healing (40.3% at 8 h and 26.2% at 24 h) and in response to the chemotactic stimulant platelet-derived growth factor-BB (38.1%). Furthermore, silencing ENaC gene expression with small interfering RNA blunted VSMC migration. These data indicate that expression of ENaC proteins is required for normal VSMC migration and suggest a potential new role for ENaC proteins in vascular tissue repair.


Gene Ontology Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 1624146
Created: 2007-05-02
Species: All species
Last Modified: 2007-05-02
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.