Ptasinska-Wnuk Dorota, Lawnicka Hanna, Mucha Slawomir, Kunert-Radek Jolanta, Pawlikowski Marek, Stepien Henryk
Department of Endocrinology, The County Hospital of Kutno, 52 Kosciuszki Street, 99-300 Kutno, Poland.
ScientificWorldJournal. 2012;2012:189290. doi: 10.1100/2012/189290. Epub 2012 Apr 24.
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.
局部肾素-血管紧张素系统存在于垂体中。我们研究了血管紧张素对体外培养的GH3催乳素生长激素细胞增殖的影响,以及p44/42和p38丝裂原活化蛋白激酶(MAPK)抑制剂在血管紧张素生长调节作用中的参与情况。材料与方法。采用Mosmann法评估细胞活力,并通过测量DNA合成过程中溴脱氧尿苷(BrdU)掺入量来评估细胞增殖。结果。血管紧张素II(Ang II)和血管紧张素IV(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,但不影响血管紧张素5-8(ang 5-8)依赖性作用。p38 MAPK抑制剂阻止了Ang-II-和Ang-IV-处理组中GH3细胞数量的减少。结论。Ang II的生长抑制作用可能由p44/42 MAPK介导。p38 MAPK似乎介导了Ang II和ang 5-8对细胞存活的抑制作用。