HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Chifflet, S. Articles by Grasso, S. Search for Related Content PubMed PubMed Citation Articles by Chifflet, S. Articles by Grasso, S.

PROTEIN AND VESICLE TRAFFICKING, CYTOSKELETON

A possible role for membrane depolarization in epithelial wound healing

¹Departamento de Bioquímica, Facultad de Medicina, and ²Sección Biofísica, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay

Submitted 27 May 2004 ; accepted in final form 17 January 2005

Linear narrow wounds produced on cultured bovine corneal endothelial monolayers heal by actin cable formation at the wound border and lamellar crawling of cells into the injured area. We report the novel finding that membrane potential depolarization occurs at the leading edge of wounds and gradually extends inward toward the neighboring cells. We have determined that the replacement of extracellular Na⁺ by choline and the incorporation of phenamil, an inhibitor of the epithelial Na⁺ channel (ENaC), provoke a decrease in the actin cable and depolarization areas and in the lamellar activity of the wound edges. To the contrary, extracellular Li⁺ can successfully replace Na⁺ in the determination of the depolarization and cytoskeletal responses. This finding supports the idea that membrane depolarization, not the increase in intracellular Na⁺ concentration, is responsible for the formation of the actin cable, a result that is in agreement with previous evidence showing that nonspecific depolarization of the plasma membrane potential (PMP) of epithelial cells may promote characteristic cytoskeletal rearrangements per se (Chifflet S, Hernández JA, Grasso S, and Cirillo A. Exp Cell Res 282: 1–13, 2003). We suggest that spontaneous depolarization of the PMP of the cells at the wound borders determined by a rise in the ENaC activity of these cells constitutes an additional factor in the intermediate cellular processes leading to wound healing in some epithelia.

actin; epithelial sodium channel

This article has been cited by other articles:

				S. C. Grifoni, S. E. McKey, and H. A. Drummond Hsc70 regulates cell surface ASIC2 expression and vascular smooth muscle cell migration Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2022 - H2030. [Abstract] [Full Text] [PDF]

				C. M. Fuller and D. J. Benos Putting the brakes on vascular smooth muscle cell migration Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H1987 - H1988. [Full Text] [PDF]

				S. C. Grifoni, K. P. Gannon, D. E. Stec, and H. A. Drummond ENaC proteins contribute to VSMC migration Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H3076 - H3086. [Abstract] [Full Text] [PDF]