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首页> 外文期刊>Life sciences >PDGF activates K-Cl cotransport through phosphoinositide 3-kinase and protein phosphatase-1 in primary cultures of vascular smooth muscle cells.
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PDGF activates K-Cl cotransport through phosphoinositide 3-kinase and protein phosphatase-1 in primary cultures of vascular smooth muscle cells.

机译：PDGF在血管平滑肌细胞的原代培养物中通过磷酸肌醇3-激酶和蛋白磷酸酶-1激活K-Cl共转运。

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摘要

K-Cl cotransport (K-Cl COT, KCC) is an electroneutrally coupled movement of K and Cl present in most cells. In this work, we studied the pathways of regulation of K-Cl COT by platelet-derived growth factor (PDGF) in primary cultures of vascular smooth muscle cells (VSMCs). Wortmannin and LY 294002 blocked the PDGF-induced K-Cl COT activation, indicating that the phosphoinositide 3-kinase (PI 3-K) pathway is involved. However, PD 98059 had no effect on K-Cl COT activation by PDGF, suggesting that the mitogen-activated protein kinase pathway is not involved under the experimental conditions tested. Involvement of phosphatases was also examined. Sodium orthovanadate, cyclosporin A and okadaic acid had no effect on PDGF-stimulated K-Cl COT. Calyculin A blocked the PDGF-stimulated K-Cl COT by 60%, suggesting that protein phosphatase-1 (PP-1) is a mediator in the PDGF signaling pathway/s. In conclusion, our results indicate that the PDGF-mediated pathways of K-Cl COT regulation involve the signaling molecules PI 3-K and PP-1.
机译：K-Cl共转运（K-Cl COT，KCC）是大多数细胞中存在的K和Cl的电中性耦合运动。在这项工作中，我们研究了在血管平滑肌细胞（VSMC）的原代培养物中血小板衍生生长因子（PDGF）对K-Cl COT的调节途径。 Wortmannin和LY 294002阻断了PDGF诱导的K-Cl COT活化，表明参与了磷酸肌醇3-激酶（PI 3-K）通路。但是，PD 98059对PDGF对K-Cl COT的激活没有影响，这表明在测试的实验条件下不涉及丝裂原激活的蛋白激酶途径。还研究了磷酸酶的参与。原钒酸钠，环孢菌素A和冈田酸对PDGF刺激的K-Cl COT无影响。 Calyculin A将PDGF刺激的K-Cl COT抑制了60％，表明蛋白磷酸酶1（PP-1）是PDGF信号通路中的介体。总之，我们的结果表明，PDGF介导的K-Cl COT调节途径涉及信号分子PI 3-K和PP-1。

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