Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes

Research output: Contribution to journalArticle

30 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)C1385-C1393
JournalAmerican Journal of Physiology - Cell Physiology
Volume269
Issue number6 38-6
StatePublished - Dec 1 1995
Externally publishedYes

Fingerprint

Corneal Keratocytes
blood serum
Cornea
cornea
acids
Serum
Flufenamic Acid
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
cells
Lysophosphatidylcholines
Osmotic Pressure
Electric potential
Amphotericin B
Ion Channels
lysophosphatidylcholine
lysophosphatidic acid
benzoic acid
fetal bovine serum
ion channels
Chemical activation

Keywords

  • New Zealand White rabbit
  • chloride channel
  • lysophosphatidylcholine
  • patch clamp
  • wound healing

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

Cite this

Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes. / Watsky, M. A.

In: American Journal of Physiology - Cell Physiology, Vol. 269, No. 6 38-6, 01.12.1995, p. C1385-C1393.

Research output: Contribution to journalArticle

@article{9c2e7808174247fa90d3a91fcfd821ca,
title = "Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes",
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.",
keywords = "New Zealand White rabbit, chloride channel, lysophosphatidylcholine, patch clamp, wound healing",
author = "Watsky, {M. A.}",
year = "1995",
month = "12",
day = "1",
language = "English (US)",
volume = "269",
pages = "C1385--C1393",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "6 38-6",

}

TY - JOUR

T1 - Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes

AU - Watsky, M. A.

PY - 1995/12/1

Y1 - 1995/12/1

N2 - 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.

AB - 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.

KW - New Zealand White rabbit

KW - chloride channel

KW - lysophosphatidylcholine

KW - patch clamp

KW - wound healing

UR - http://www.scopus.com/inward/record.url?scp=0029189983&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029189983&partnerID=8YFLogxK

M3 - Article

C2 - 8572167

AN - SCOPUS:0029189983

VL - 269

SP - C1385-C1393

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 6 38-6

ER -