Lysophosphatidic acid, serum and hyposmolarity activate cl-
currents in corneal keratocytes.
Watsky, Mitchell A.
Department of Physiology and Biophysics, University of Tennessee,
Memphis, Tennessee 38163
APStracts 2:0246C, 1995.
The influence of serum, lysophosphatidic acid (LPA), and hyposmotic
stress on the ion channel activity of normal and cryo-injured rabbit
corneal keratocytes was investigated. Whole-cell currents were
examined using the amphotericin perforated-patch technique. In cells
from wounded corneas, fetal bovine serum activated large, holding
voltage insensitive, fast activating, DIDS, flufenamic acid and NPPB
blockable outward currents showing inactivation at depolarized
voltages. LPA activated identical currents, also only in cells from
wounded corneas. Blocker and reversal potential experiments
characterized the current as a Cl- current (ICl-).
Lysophosphatidylcholine (10 [mu]M) failed to activate the current. An
identical current was activated by hyposmotic stimulation in cells
from control and wounded corneas. Hyposmotic strimulation also
activated ICl- in cells from wounded corneas that were unresponsive
to LPA. We conclude that serum, LPA and hypotonic stress activate
ICl- in keratocytes from wounded corneas. We also conclude that LPA
is a serum factor that can activate ICl-, and that hyposmotic
activation may work through a signaling pathway separate from that of
LPA.
Received 10 March 1995; accepted in final form 23 May 1995
APS Manuscript Number C0137-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.