Abstract
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 μM) 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.
Original language | English (US) |
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Pages (from-to) | C1385-C1393 |
Journal | American Journal of Physiology - Cell Physiology |
Volume | 269 |
Issue number | 6 38-6 |
DOIs | |
State | Published - 1995 |
Externally published | Yes |
Keywords
- New Zealand White rabbit
- chloride channel
- lysophosphatidylcholine
- patch clamp
- wound healing
ASJC Scopus subject areas
- Physiology
- Cell Biology