Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes
Watsky, M.A.
American Journal of Physiology 269(6 Pt 1): C1385-C1393
1995
ISSN/ISBN: 0002-9513 PMID: 8572167 Document Number: 441659
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, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-, flufenamic acid-, and 5-nitro-2-(3-phenylpropylamino)benzoic acid (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 (I-Cl). 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 stimulation also activated I-Cl in cells from wounded corneas that were unresponsive to LPA. We conclude that serum, LPA, and hypotonic stress activate I-Cl in keratocytes from wounded corneas. We also conclude that LPA is a serum factor that can activate I-Cl and that hyposmotic activation may work through a signaling pathway separate from that of LPA.