title: ENaC contribution to epithelial wound healing is independent of the healing mode and of any increased expression in the channel.
abstract: Previous work from our laboratory and others has shown that, in some epithelia, the epithelial sodium channel (ENaC) increases its expression during wound healing. In these cases, inhibition of the channel determines a decrease in the healing rate, a result suggesting a role for ENaC in the overall healing process. To understand further this role of ENaC in epithelia, we explored the participation of ENaC in wound healing in four cultured epithelial cell lines selected on the basis of their different embryonic origins, function and modality of healing, i.e., by lamellipodial cell crawling or by actin cable formation. Three of the cell lines (bovine corneal endothelial cells, rabbit corneal epithelial cells and Madin-Darby canine kidney cells) exhibited an increase in ENaC expression and consequent membrane potential depolarization and an increase in cytosolic sodium and calcium, whereas one line (bovine aortal endothelial cells, BAEC) did not exhibit any of these changes. In all of the cell lines, however, ENaC inhibition determined a similar decrease in the rate of wound healing. In BAEC monolayers, the increase in ENaC activity produced plasma membrane depolarization, increased cytosolic sodium and calcium, and augmented the velocity of healing. These novel findings contribute to the idea that ENaC plays a critical role in wound healing in various epithelia, independently of the modality of healing and of any increase in the expression of the channel.
authors: Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Gral. Flores 2125, 11800, Montevideo, Uruguay.
authors: Cristian
authors: C
authors: Justet
authors: Frances
authors: F
authors: Evans
authors: Elena
authors: E
authors: Vasilskis
authors: Julio A
authors: JA
authors: Hernández
authors: Silvia
authors: S
authors: Chifflet
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001013:Aorta, Thoracic / Q000166:cytology / Q000293:injuries / Q000378:metabolism*; D002417:Cattle; D002460:Cell Line; D005576:Colforsin / Q000494:pharmacology; D003315:Cornea / Q000166:cytology / Q000378:metabolism*; D065306:Corneal Injuries; D004285:Dogs; D004847:Epithelial Cells / Q000378:metabolism; D062686:Epithelial Sodium Channel Blockers / Q000494:pharmacology; D053503:Epithelial Sodium Channels / Q000096:biosynthesis / Q000378:metabolism*; D004848:Epithelium / Q000276:immunology / Q000378:metabolism; D006096:Gramicidin / Q000494:pharmacology; D061985:Madin Darby Canine Kidney Cells; D008564:Membrane Potentials / Q000502:physiology; D011817:Rabbits; D014665:Vasodilator Agents / Q000494:pharmacology; D014945:Wound Healing / Q000502:physiology*
chemical_list: D000900:Anti-Bacterial Agents; D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels; D014665:Vasodilator Agents; D006096:Gramicidin; D005576:Colforsin