Nonselective cation channel activation during wound healing in the corneal
endothelium.
Watsky, Mitchell A., Ph.d.
Department of Physiology and Biophysics, The University of Tennessee,
Memphis, 38163
APStracts 2:0043C, 1995.
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
post-wounding, 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 freeze wounded endothelial cells 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.
Received 22 August 1994; accepted in final form 30 November 1994
APS Manuscript Number C0497-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.