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首页> 外文期刊>Biology of Reproduction: Offical Journal of the Society for the Study of Reproduction >Plasminogen activator inhibitor 1 RNA-binding protein interacts with progesterone receptor membrane component 1 to regulate progesterone's ability to maintain the viability of spontaneously immortalized granulosa cells and rat granulosa cells.
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Plasminogen activator inhibitor 1 RNA-binding protein interacts with progesterone receptor membrane component 1 to regulate progesterone's ability to maintain the viability of spontaneously immortalized granulosa cells and rat granulosa cells.

机译：纤溶酶原激活物抑制剂1 RNA结合蛋白与孕激素受体膜成分1相互作用，调节孕酮维持自发永生的颗粒细胞和大鼠颗粒细胞活力的能力。

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摘要

Progesterone receptor membrane component 1 (PGRMC1) mediates the antiapoptotic action of progesterone (P4). PGRMC1 interacts with plasminogen activator inhibitor 1 RNA-binding protein (PAIRBP1), but the functional significance of this interaction is unknown. To examine the function of PGRMC1-PAIRBP1 interaction, PAIRBP1 was depleted from spontaneously immortalized granulosa cells (SIGCs) and the effects on the expression and localization of PGRMC1 as well as P4's ability to bind to SIGCs and prevent apoptosis was assessed. Depleting PAIRBP1 enhanced cellular (3)H-P4 binding and did not alter the expression or cellular localization of PGRMC1 but attenuated P4's antiapoptotic action. Transfection of a PGRMC1-green fluorescent protein (GFP) peptide mimic, which binds PAIRBP1 as demonstrated by in situ proximity assay, doubled the rate at which SIGCs undergo apoptosis compared to cells transfected with either the empty GFP expression vector or Pairbp1 small interfering RNA. Moreover, P4 did not prevent these cells from undergoing apoptosis. Similar studies conducted with granulosa cells isolated from immature rats also showed that PGRMC1 interacts with PAIRBP1 and that transfection of PGRMC1-GFP peptide mimic accelerates the rate of granulosa cell apoptosis by 4-fold even in the presence of serum and P4. These studies support the concept that the interaction between PAIRBP1-PGRMC1 is an essential component of the mechanism through which P4 inhibits apoptosis. Surprisingly, PGRMC1-PAIRBP1 interaction is not required for P4 binding or the cellular localization of PGRMC1 but rather appears to couple PGRMC1 to downstream components of the P4-PGRMC1 signal transduction pathway.
机译：孕酮受体膜成分1（PGRMC1）介导孕酮（P4）的抗凋亡作用。 PGRMC1与纤溶酶原激活物抑制剂1 RNA结合蛋白（PAIRBP1）相互作用，但这种相互作用的功能意义尚不清楚。为了检查PGRMC1-PAIRBP1相互作用的功能，从自发永生的颗粒细胞（SIGC）中清除了PAIRBP1，并评估了对PGRMC1表达和定位的影响以及P4结合SIGC和防止细胞凋亡的能力。耗尽PAIRBP1增强了细胞（3）H-P4的结合，并没有改变PGRMC1的表达或细胞定位，但减弱了P4的抗凋亡作用。如通过原位邻近分析证实的那样，结合了PAIRBP1的PGRMC1-绿色荧光蛋白（GFP）肽模拟物的转染，与用空GFP表达载体或Pairbp1小干扰RNA转染的细胞相比，SIGC发生细胞凋亡的速度增加了一倍。而且，P4不能阻止这些细胞凋亡。对从未成熟大鼠中分离出的颗粒细胞进行的类似研究还显示，PGRMC1与PAIRBP1相互作用，PGRMC1-GFP肽模拟物的转染即使在存在血清和P4的情况下，也可以使颗粒细胞凋亡的速率提高4倍。这些研究支持以下观念：PAIRBP1-PGRMC1之间的相互作用是P4抑制细胞凋亡的机制的重要组成部分。出人意料的是，PGRMC1-PAIRBP1相互作用不是P4结合或PGRMC1的细胞定位所必需的，而是似乎将PGRMC1与P4-PGRMC1信号转导途径的下游组分偶联。

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