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Am J Physiol Heart Circ Physiol (July 14, 2006). doi:10.1152/ajpheart.00333.2006
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Submitted on March 29, 2006
Accepted on July 12, 2006

ENaC PROTEINS CONTRIBUTE TO VSMC MIGRATION

Samira de Campos Grifoni1, Kimberly Anita Gannon1, David E. Stec1, and Heather A Drummond1*

1 Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States

* To whom correspondence should be addressed. E-mail: hdrummond{at}physiology.umsmed.edu.

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 ENaC inhibition abolishes pressure-induced constriction in isolated artery segments. However, it is unknown if ENaC proteins play a role in VSMC migration. The goal of this study was to determine if ENaC molecules are required for VSMC migration. Using RT-PCR, immuno-blotting and -labeling, we detected expression of {alpha}, {beta} and {gamma} ENaC transcripts and proteins in cultured VSMCs (SV40LT-SMC and A10 cells). Of the three proteins, {beta} ENaC was the most readily detected in both cell lines by immunolocalization and Western blotting. Inhibition of ENaC activity with 1 µM benzamil blunted VSMC migration associated with wound healing (40.3% at 8 hr and 26.2% at 24 hr) and in response to the chemotactic stimulant PDGF-bb (38.1%). Furthermore, silencing ENaC gene expression with siRNA blunted VSMC migration. These data indicate expression of ENaC proteins are required for normal VSMC migration and suggest a potential new role for ENaC proteins in vascular tissue repair.




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