首页> 美国卫生研究院文献>The Scientific World Journal >Angiotensins Inhibit Cell Growth in GH3 Lactosomatotroph Pituitary Tumor Cell Culture: A Possible Involvement of the p44/42 and p38 MAPK Pathways
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Angiotensins Inhibit Cell Growth in GH3 Lactosomatotroph Pituitary Tumor Cell Culture: A Possible Involvement of the p44/42 and p38 MAPK Pathways

机译:血管紧张素抑制GH3乳突营养腺垂体肿瘤细胞培养中的细胞生长:p44 / 42和p38 MAPK途径的可能参与

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摘要

The local renin-angiotensin system is present in the pituitary. We investigated the effects of angiotensins on GH3 lactosomatotroph cells proliferation in vitro and the involvement of p44/42 and p38 MAPK inhibitors in the growth-regulatory effects of angiotensins. Materials and Methods. Cell viability using the Mosmann method and proliferation by the measurement of BrdU incorporation during DNA synthesis were estimated. Results. Ang II and ang IV decreased the viability and proliferation of GH3 cells. Inhibitor of p44/42 MAPK attenuated the effects of ang II on cell viability and proliferation but did not affect the ang 5-8-dependent actions. Inhibitor of p38 MAPK prevented the decrease in the number of GH3 cells in ang-II- and ang-IV-treated groups. Conclusions. The growth-inhibitory effect of ang II is possibly mediated by the p44/42 MAPK. The p38 MAPK appears to mediate the inhibitory effects of both ang II and ang 5–8 upon cell survival.
机译:垂体中存在局部的肾素-血管紧张素系统。我们调查了血管紧张素对GH3乳突营养细胞增殖的影响,以及p44 / 42和p38 MAPK抑制剂在血管紧张素的生长调节作用中的作用。材料和方法。使用Mosmann方法评估细胞活力,并通过在DNA合成过程中测量BrdU掺入来评估其增殖。结果。 Ang II和Ang IV降低了GH3细胞的活力和增殖。 p44 / 42 MAPK抑制剂减弱了ang II对细胞活力和增殖的影响,但不影响ang 5-8依赖性作用。 p38 MAPK抑制剂可防止ang-II和ang-IV治疗组的GH3细胞数量减少。结论。 Ang II的生长抑制作用可能是由p44 / 42 MAPK介导的。 p38 MAPK似乎介导了ang II和ang 5-8对细胞存活的抑制作用。

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