The ERK Signaling Cascade Inhibits Gonadotropin-Stimulated Steroidogenesis.

Rony Seger, Tamar Hanoch, Revital Rosenberg, Ada Dantes, Wolfgang E Merz, Jerome F Strauss, Abraham Amsterdam
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引用次数: 27

Abstract

The response of granulosa cells to Luteinizing Hormone (LH) and Follicle- Stimulating Hormone (FSH) is mediated mainly by cAMP/protein kinase A (PKA) signaling. Notably, the activity of the extracellular signal-regulated kinase (ERK) signaling cascade is elevated in response to these stimuli as well. We studied the involvement of the ERK cascade in LH- and FSH-induced steroidogenesis in two granulosa-derived cell lines, rLHR-4 and rFSHR-17, respectively. We found that stimulation of these cells with the appropriate gonadotropin induced ERK activation as well as progesterone production downstream of PKA. Inhibition of ERK activity enhanced gonadotropin-stimulated progesterone production, which was correlated with increased expression of the Steroidogenic Acute Regulatory Protein (StAR), a key regulator of progesterone synthesis. Therefore, it is likely that gonadotropin-stimulated progesterone formation is regulated by a pathway that includes PKA and StAR, and this process is down-regulated by ERK, due to attenuation of StAR expression. Our results suggest that activation of PKA signaling by gonadotropins not only induces steroidogenesis but also activates down-regulation machinery involving the ERK cascade. The activation of ERK by gonadotropins as well as by other agents may be a key mechanism for the modulation of gonadotropin-induced steroidogenesis.

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ERK信号级联抑制促性腺激素刺激的类固醇生成。
颗粒细胞对促黄体生成素(LH)和促卵泡激素(FSH)的反应主要由cAMP/蛋白激酶A (PKA)信号介导。值得注意的是,细胞外信号调节激酶(ERK)信号级联的活性在这些刺激下也会升高。我们研究了ERK级联在LH和fsh诱导的两种颗粒来源细胞系rLHR-4和rFSHR-17中的参与作用。我们发现用适当的促性腺激素刺激这些细胞可诱导ERK活化以及PKA下游的孕酮产生。抑制ERK活性可增强促性腺激素刺激的孕激素产生,这与类固醇急性调节蛋白(StAR)的表达增加有关,StAR是孕激素合成的关键调节因子。因此,促性腺激素刺激的孕酮形成很可能受到包括PKA和StAR在内的一条通路的调控,而由于StAR表达的衰减,这一过程被ERK下调。我们的研究结果表明,促性腺激素激活PKA信号不仅可以诱导类固醇生成,还可以激活涉及ERK级联的下调机制。促性腺激素以及其他药物对ERK的激活可能是调节促性腺激素诱导的类固醇生成的关键机制。
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