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首页> 外文期刊>Journal of Cellular Physiology >Activation of P2Y2 receptor induces c-FOS protein through a pathway involving mitogen-activated protein kinases and phosphoinositide 3-kinases in HeLa cells.
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Activation of P2Y2 receptor induces c-FOS protein through a pathway involving mitogen-activated protein kinases and phosphoinositide 3-kinases in HeLa cells.

机译：激活P2Y2受体诱发c-FOS蛋白质通过一个涉及增殖作用的途径蛋白激酶和磷酸肌醇3-kinases

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The effects of P2Y2 purinoceptor activation on c-Fos expression and the signaling pathways evoked by extracellular ATP/UTP in HeLa cells were investigated. We found that P2Y2 activation induced c-Fos protein and phosphorylated the extracellular signal-regulated kinases 1 and 2 (ERK1/2). The P2Y2-stimulated c-Fos induction was partly blocked (a) by U73122, a phospholipase C inhibitor, (b) by Go6976, a conventional PKC inhibitor, (c) by PD098059, a mitogen-activated protein kinase kinase inhibitor, and, moreover, (d) by the inhibitors of phosphoinositide 3-kinases (PI3K), LY294002 and wortmannin. When Go6976 and PD098059, or Go6976 and wortmannin, were combined there was a totally inhibition of P2Y2-induced c-Fos increase. Either U73122 or Go6976 did not inhibit ERK1/2 phosphorylation induced by ATP/UTP, while it was inhibited by LY294002 (or wortmannin) and by staurosporine. Additionally, wortmannin inhibited the cytosol-to-membrane translocation of PKC- varepsilon induced by ATP/UTP. These data indicated that agonist-induced PI3K and downstream PKC- varepsilon activation mediated the effect of ATP/UTP on ERK1/2 activation. To test the biological consequences of ERK1/2 activation, the effect of P2Y2 on cell functions were examined. P2Y2 stimulation increased cell proliferation and this effect was attenuated by PD098059 in a dose-dependent manner, thereby indicating that the ERK pathway mediates mitogenic signaling by P2Y2. In conclusion, the activation of conventional PKCs through P2Y2 receptor acts in concert with ERK and PI3K/PKC- varepsilon pathways to induce c-Fos protein and HeLa cell proliferation.
机译：的影响P2Y2 purinoceptor激活c-Fos表达和信号通路诱发细胞外ATP / UTP海拉细胞被调查。诱导c-Fos蛋白质及磷酸化细胞外signal-regulated激酶1和2(ERK1/2)。由U73122部分阻塞(a),磷脂酶CGo6976抑制剂,(b)的传统PKCPD098059抑制剂,(c)的增殖作用此外,蛋白激酶激酶抑制剂,(d)的抑制剂磷酸肌醇3-kinases (PI3K) LY294002和渥曼青霉素。Go6976 PD098059,或Go6976渥曼青霉素,结合的完全抑制吗P2Y2-induced c-Fos增加。Go6976没有抑制ERK1/2磷酸化引起ATP / UTP,同时抑制了由staurosporine LY294002(或渥曼青霉素)和。此外,渥曼青霉素抑制了cytosol-to-membrane易位的PKC -varepsilon引起ATP / UTP。表明agonist-induced PI3K和下游PKC - varepsilon激活介导ATP / UTP ERK1/2激活的影响。测试生物ERK1/2的后果激活,P2Y2对细胞功能的影响被检查。核扩散和这种效应减弱了PD098059剂量依赖性的方式,从而表明ERK通路介导由P2Y2促有丝分裂的信号。通过P2Y2激活传统PKCs的受体的行为符合ERK和PI3K / PKC -varepsilon诱导c-Fos蛋白质和途径海拉细胞增殖。

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