Adhesion is required for protein kinase C-dependent activation of the Na+/H+ antiporter by platelet-derived growth factor.

Adhesion is required for protein kinase C-dependent activation of the Na+/H+ antiporter by platelet-derived growth factor.
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血小板衍生生长因子依赖蛋白激酶 C 激活 Na /H 逆向转运蛋白,需要粘附作用。

DOI:
10.1073/pnas.89.13.6138
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发表时间:
1992
影响因子:
11.1
通讯作者:
Lechene,C
Lechene,C
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Schwartz,MA;Lechene,C

文献摘要

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正常的贴壁依赖性细胞粘附到固体基质上导致Na+/H+反向转运蛋白的激活和细胞内pH值的升高。这些作用由细胞外基质蛋白(如纤连蛋白)及其受体(整合素)介导。在C3 H 10 T1/2细胞中使用蛋白激酶C(PKC)的药理学抑制和下调的实验表明,血小板衍生生长因子通过PKC依赖性途径在粘附细胞中诱导Na+/H+反向转运蛋白的活化,但在粘附性差的细胞中不能这样做。然而,粘附性差的细胞能够响应佛波醇酯而升高细胞内pH,这表明PKC和该途径中的后续步骤是功能性的。这些结果表明,偶联血小板衍生生长因子PKC激活需要细胞粘附。
Adhesion of normal, anchorage-dependent cells to a solid substratum leads to activation of the Na+/H+ antiporter and elevation of intracellular pH. These effects are mediated by extracellular matrix proteins, such as fibronectin, and their receptors, the integrins. Experiments using pharmacological inhibition and down-regulation of protein kinase C (PKC) in C3H 10T1/2 cells show that platelet-derived growth factor induces activation of the Na+/H+ antiporter by means of a PKC-dependent pathway in adherent cells but cannot do so in poorly adherent cells. Poorly adherent cells are, however, able to elevate intracellular pH in response to a phorbol ester, indicating that PKC and subsequent steps in the pathway are functional. These results indicate that coupling of platelet-derived growth factor to PKC activation requires cell adhesion.