Ohmichi M, Koike K, Nohara A, Kanda Y, Sakamoto T, Zhang Z X, Hirota K, Miyake A
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
Biochem Biophys Res Commun. 1994 Jun 15;201(2):642-8. doi: 10.1006/bbrc.1994.1749.
We recently reported the existence of two separate pathways for thyrotropin-releasing hormone (TRH)-induced mitogen-activated protein (MAP) kinase activation in GH3 pituitary tumor cells. To test the role of MAP kinase in TRH action, we examined the effect of dopamine (DA) on TRH-induced MAP kinase in primary cultures of rat anterior pituitary cells. 1 microM of DA attenuated 1 microM TRH-induced MAP kinase activity and phosphorylation. 100 ng/ml of islet-activating protein (IAP) blocked these inhibitory effects of DA. These results suggest that crosstalk exists between the DA signaling pathway and the TRH-stimulated MAP kinase activating pathway in rat anterior pituitary cells.
我们最近报道，在GH3垂体瘤细胞中，促甲状腺激素释放激素（TRH）诱导的丝裂原活化蛋白（MAP）激酶激活存在两条独立的途径。为了测试MAP激酶在TRH作用中的作用，我们研究了多巴胺（DA）对原代培养的大鼠垂体前叶细胞中TRH诱导的MAP激酶的影响。1微摩尔的DA减弱了1微摩尔TRH诱导的MAP激酶活性和磷酸化。100纳克/毫升的胰岛激活蛋白（IAP）阻断了DA的这些抑制作用。这些结果表明，在大鼠垂体前叶细胞中，DA信号通路与TRH刺激的MAP激酶激活通路之间存在相互作用。
