PGRMC1 and PGRMC2 in uterine physiology and disease.
PGRMC1 and PGRMC2 in uterine physiology and disease.
复制标题
DOI：
10.3389/fnins.2013.00168
复制
发表时间：
2013
影响因子：
4.3
通讯作者：
Clark NC
中科院分区：
文献类型：
--
作者：
Pru JK;Clark NC
从使用孕酮受体（PGR）突变小鼠的研究中可以清楚地看出，并非孕酮（P4）的所有作用都是由该受体介导的。事实上，许多快速的，非经典的P4行动已报告整个女性生殖道。Pgr基因缺失小鼠的预后治疗导致行为变化和子宫内膜中基因的差异调节。孕激素受体膜成分（PGRMC）1和PGRMC 2属于血红素结合蛋白家族，可能作为P4受体。支持这一点的证据主要来自使用缺乏经典PCR的原代或转化细胞系的体外培养工作。PGRMC 1在月经周期哺乳动物中的子宫内膜表达在周期的增殖期最丰富。由于PGRMC 2表达显示出最一致的跨物种表达，在分泌期具有最高水平，因此PGRMC 2可作为子宫中的通用非经典P4受体。虽然PGRMC 1/2在子宫中的功能重要性仍有待充分研究，但越来越多的证据表明PGRMC 1/2表达的中断与子宫疾病相关。在这篇综述中，我们将总结什么是已知的PGRMC 1/2在子宫生理学，我们将提供这些基因在子宫疾病状态下的表达中断的例子。
It is clear from studies using progesterone receptor (PGR) mutant mice that not all of the actions of progesterone (P4) are mediated by this receptor. Indeed, many rapid, non-classical P4 actions have been reported throughout the female reproductive tract. Progesterone treatment of Pgr null mice results in behavioral changes and in differential regulation of genes in the endometrium. Progesterone receptor membrane component (PGRMC) 1 and PGRMC2 belong to the heme-binding protein family and may serve as P4 receptors. Evidence to support this derives chiefly from in vitro culture work using primary or transformed cell lines that lack the classical PGR. Endometrial expression of PGRMC1 in menstrual cycling mammals is most abundant during the proliferative phase of the cycle. Because PGRMC2 expression shows the most consistent cross-species expression, with highest levels during the secretory phase, PGRMC2 may serve as a universal non-classical P4 receptor in the uterus. While the functional importance of PGRMC1/2 in the uterus remains to be fully explored, accumulating evidence suggests that disruption in PGRMC1/2 expression correlates with uterine disease. In this review we will summarize what is known about PGRMC1/2 in uterine physiology and we will provide examples of disrupted expression of these genes in uterine disease states.
登录
查看更多内容
影响因子：
2.4
作者：
Boruban, Melih C.;Altundag, Kadri;Blankstein, Josef
通讯作者：
Blankstein, Josef
影响因子：
4.4
作者：
Chen, Jenny I-C.;Hannan, Natalie J.;Stephens, Andrew N.
通讯作者：
Stephens, Andrew N.
影响因子：
2.7
作者：
Albrecht, Christian;Huck, Volker;Wendler, Alexandra
通讯作者：
Wendler, Alexandra
影响因子：
3.3
作者：
Intlekofer, K. A.;Petersen, S. L.
通讯作者：
Petersen, S. L.
影响因子：
3.6
作者：
Dunlap, KA;Stormshak, F
通讯作者：
Stormshak, F