Nonselective cation channel activation during wound healing in the corneal endothelium.
Rabbit corneas were injured by mechanical or thermal trauma. At several time points after wounding, corneal endothelial cells were isolated and their ion channels examined using standard and amphotericin perforated-patch whole cell patch-clamp configurations. Within 15-24 h after mechanical or thermal trauma, a nonselective cation current was observed in 79% of the cells examined that was not present in unwounded or sham-wounded corneas. By 73 h postwounding, the current was present in only 10% of the cells examined. The wound healing-induced current is outwardly rectifying, activates at depolarized voltages, shows no sign of inactivation, and is inhibited by flufenamic acid, quinidine, and acetate. In addition to this new current, it was observed that endothelial cells from freeze-wounded corneas no longer expressed the transient K+ current seen in control, sham, and mechanically wounded corneas. Corneal endothelial superfusion experiments found no significant difference in swelling rates between control and flufenamic acid-superfused wounded corneas, indicating that the wound healing-induced channel is not involved in the stromal hydration maintenance function of the corneal endothelium.
Watsky
M A
MA
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163, USA.
D000818:Animals; D002412:Cations / Q000378:metabolism*; D004594:Electrophysiology; D004728:Endothelium, Corneal / Q000473:pathology / Q000502:physiology*; D007473:Ion Channels / Q000378:metabolism*; D010477:Perfusion / Q000379:methods; D011817:Rabbits; D014945:Wound Healing / Q000502:physiology*
D002412:Cations; D007473:Ion Channels