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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Connexins and steroidogenesis in mouse Leydig cells
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Connexins and steroidogenesis in mouse Leydig cells

机译：小鼠Leydig细胞中的连接蛋白和类固醇生成

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摘要

Connexin43 has been recognized as forming gap junctions in Leydig cells. However, previous work has shown that mouse Leydig cells lacking this connexin do not suffer any limitation of their ability to produce testosterone when stimulated with luteinizing hormone. The objective of this study was to identify additional connexins in mouse Leydig cells that could be required for steroidogenesis. A reverse transcription - polymerase chain reaction screen involving isolated adult Leydig cells identified connexin36 and connexin45 as expressed along with connexin43. Treatment of dissociated testes with carbenoxolone, a nonspecific blocker of gap junctional coupling, significantly reduced testosterone output as did treatment with quinine, which disrupts coupling provided by connexin36 and connexin45 gap junctions but not those composed of connexin43, indicating that either or both of connexins 36 and 45 could be involved in supporting Leydig cell steroidogenesis. Immunolabeling of adult mouse testis sections confirmed the localization of connexin36 along with connexin43 in Leydig cell gap junctions but not connexin45, which is distributed throughout the cells. It was concluded that connexin36, connexin43, and connexin45 are coexpressed in Leydig cells with connexins 36 and 43 contributing to gap junctions. The role of connexin45 remains to be elucidated.
机译：连接蛋白43已经被认为在Leydig细胞中形成间隙连接。但是，先前的研究表明，缺乏这种连接蛋白的小鼠Leydig细胞在受到黄体生成素刺激时，其产生睾丸激素的能力不受任何限制。这项研究的目的是确定类固醇生成所需的小鼠Leydig细胞中的其他连接蛋白。涉及分离的成年Leydig细胞的逆转录-聚合酶链反应筛选鉴定出与连接蛋白43一起表达的连接蛋白36和连接蛋白45。与奎宁处理一样，用缝隙连接偶联的非特异性阻断剂羧苄索隆治疗解离的睾丸，可显着降低睾丸激素输出，奎宁治疗可破坏连接蛋白36和连接蛋白45的缝隙连接，但不破坏连接蛋白43的连接，表明连接蛋白36中的一个或全部45个可能参与支持Leydig细胞类固醇生成。成年小鼠睾丸切片的免疫标记证实了连接蛋白36和连接蛋白43在Leydig细胞间隙连接处的定位，但不是连接蛋白45的定位，其分布在整个细胞中。结论是，连接蛋白36，连接蛋白43和连接蛋白45在Leydig细胞中共表达，其中连接蛋白36和43有助于间隙连接。连接蛋白45的作用尚待阐明。

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