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首页> 外文期刊>Cytokine >The adiponectin paralog C1q/TNF-related protein 3 (CTRP3) stimulates testosterone production through the cAMP/PKA signaling pathway
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The adiponectin paralog C1q/TNF-related protein 3 (CTRP3) stimulates testosterone production through the cAMP/PKA signaling pathway

机译：脂联素旁系同源C1q / TNF相关蛋白3（CTRP3）通过cAMP / PKA信号通路刺激睾丸激素的产生

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摘要

CTRP3, a paralog of adiponectin, is a member of the C1q and tumor necrosis factor (TNF)-related protein (CTRP) superfamily. It is expressed at high levels in adipose tissue and has recently emerged as a novel adipokine. In the present study, we provide the first evidence for a physiological role of the new adipokine, CTRP3, in the reproductive system. CTRP3 was specifically expressed in interstitial Leydig cells, where testosterone is produced, in the adult mouse testis. CTRP3 increased testosterone production by TM3 mouse Leydig cells in a dose-dependent manner. The increased testosterone production was linked to upregulation of steroidogenic proteins expression, such as steroidogenic acute regulatory (StAR) protein and cholesterol side-chain cleavage cytochrome P450 (P450scc). Moreover, increases in intracellular cyclic AMP (cAMP) concentrations and the phosphorylation of cAMP-response element binding protein (CREB) in CTRP3-stimulated TM3 Leydig cells were observed. Inhibition of this signaling pathway by a specific protein kinase A (PKA) inhibitor, H89, blocked testosterone production in CTRP3-stimulated Leydig cells, suggesting that the stimulatory effect of CTRP3 on testosterone production is associated with activation of the cAMP/PKA signaling pathway. Thus, our results demonstrate a physiological role for CTRP3 in testicular steroidogenesis and provide novel insights in the intracellular mechanisms activated by this protein.
机译：CTRP3是脂联素的旁系同源物，是C1q和肿瘤坏死因子（TNF）相关蛋白（CTRP）超家族的成员。它在脂肪组织中高水平表达，近来已成为一种新型的脂肪因子。在本研究中，我们提供了新的脂肪因子CTRP3在生殖系统中的生理作用的第一个证据。 CTRP3在成年小鼠睾丸中的间质Leydig细胞中特异性表达，该细胞在其中产生睾丸激素。 CTRP3以剂量依赖性方式增加了TM3小鼠Leydig细胞产生的睾丸激素。睾丸激素产生的增加与类固醇生成蛋白表达的上调相关，例如类固醇生成急性调节（StAR）蛋白和胆固醇侧链裂解细胞色素P450（P450scc）。此外，观察到在CTRP3刺激的TM3 Leydig细胞中细胞内环AMP（cAMP）浓度增加和cAMP反应元件结合蛋白（CREB）磷酸化。特定的蛋白激酶A（PKA）抑制剂H89对该信号通路的抑制作用阻断了CTRP3刺激的Leydig细胞中睾丸激素的产生，这表明CTRP3对睾丸激素产生的刺激作用与cAMP / PKA信号通路的激活有关。因此，我们的结果证明了CTRP3在睾丸类固醇生成中的生理作用，并为该蛋白激活的细胞内机制提供了新的见解。

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