Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes.
Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes.
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DOI：
10.1152/ajpcell.1995.269.6.c1385
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发表时间：
1995-12
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影响因子：
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通讯作者：
M. Watsky
中科院分区：
文献类型：
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作者：
M. Watsky
研究了血清、溶血磷脂酸（LPA）和低渗应激对正常和冷冻损伤兔角膜基质细胞离子通道活性的影响。全细胞电流进行了检查，使用的阿替西霉素穿孔贴片技术。在来自受伤角膜的细胞中，胎牛血清激活大的、保持电压不敏感的、快速激活的、4，4 '-二异硫氰基芪-2，2'-二磺酸（DIDS）-、氟灭酸-和5-硝基-2-（3-苯丙基氨基）苯甲酸（NPPB）-可阻断的外向电流，其在去极化电压下显示失活。LPA激活了相同的电流，也只在受伤的角膜细胞中。阻断剂和反转电位实验将电流表征为Cl-电流（Icl）。溶血磷脂酰胆碱（10 μ M）未能激活电流。在对照组和受伤角膜的细胞中，低渗刺激激活了相同的电流。低渗刺激也激活了对LPA无反应的受伤角膜细胞中的Icl。我们的结论是血清，LPA，低渗应力激活角膜细胞从受伤的角膜。我们还得出结论，LPA是一种血清因子，可以激活Icl和低渗激活可能通过一个信号通路分离的LPA。
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- currents (Icl). Lysophosphatidylcholine (10 microM) failed to activate the current. An identical current was activated by hyposmotic stimulation in cells from control and wounded corneas. Hyposmotic stimulation 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.