Morris J K, Richards J S
Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030.
Endocrinology. 1995 Apr;136(4):1549-58. doi: 10.1210/endo.136.4.7895665.
The LH surge induces ovulation [prostaglandin synthase-2 (PGS-2)] and luteinization (progesterone synthesis) of preovulatory follicles by cAMP-dependent mechanisms. Peptides, such as GnRH and angiotensin-II, that activate other cellular signaling pathways have been shown to mimic some of the effects of LH. Therefore, the relative functional importance of different cellular signaling pathways in mediating the induction of PGS-2 and luteinization was analyzed using the agonists (LH, GnRH, and angiotensin-II) and selective inhibitors of A-kinase (H-89), C-kinase (calphostin-C), and calmodulin kinase-II (KN93). LH or GnRH, but not angiotensin-II, markedly induced PGS-2 protein in preovulatory follicles. H-89 and calphostin-C, but not KN93 inhibited LH induction of PGS-2, whereas calphostin-C selectively blocked induction by GnRH. In contrast, the A- and C-kinase inhibitors prevented both LH and GnRH induction of granulosa cell luteinization. Taken together, these results provide biological evidence that the response of granulosa cells to the LH surge appears to involve the activation of A- and C-kinase pathways.
促黄体生成素（LH）峰通过环磷酸腺苷（cAMP）依赖性机制诱导排卵前卵泡排卵[前列腺素合成酶-2（PGS-2）]和黄素化（孕酮合成）。已表明，激活其他细胞信号通路的肽，如促性腺激素释放激素（GnRH）和血管紧张素II，可模拟LH的某些作用。因此，使用激动剂（LH、GnRH和血管紧张素II）以及A激酶（H-89）、C激酶（钙磷蛋白-C）和钙调蛋白激酶II（KN93）的选择性抑制剂，分析了不同细胞信号通路在介导PGS-2诱导和黄素化中的相对功能重要性。LH或GnRH可显著诱导排卵前卵泡中的PGS-2蛋白，但血管紧张素II则不能。H-89和钙磷蛋白-C可抑制LH对PGS-2的诱导，但KN93不能，而钙磷蛋白-C可选择性阻断GnRH的诱导。相反，A激酶和C激酶抑制剂可同时阻止LH和GnRH诱导颗粒细胞黄素化。综上所述，这些结果提供了生物学证据，表明颗粒细胞对LH峰的反应似乎涉及A激酶和C激酶途径的激活。
