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首页> 外文期刊>American Journal of Physiology >Nuclear progesterone receptor A and B isoforms in mouse fallopian tube and uterus: implications for expression, regulation, and cellular function.
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Nuclear progesterone receptor A and B isoforms in mouse fallopian tube and uterus: implications for expression, regulation, and cellular function.

机译：小鼠输卵管和子宫中的核孕酮受体A和B同工型：对表达，调节和细胞功能的影响。

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Progesterone and its interaction with nuclear progesterone receptors (PR) PR-A and PR-B play a critical role in the regulation of female reproductive function in all mammals. However, our knowledge of the regulation and possible cellular function of PR protein isoforms in the fallopian tube and uterus in vivo is still very limited. In the present study, we revealed that equine chorionic gonadotropin (eCG) treatment resulted in a time-dependent increase in expression of both isoforms, reaching a maximal level at 48 h in the fallopian tube. Regulation of PR-A protein expression paralleled that of PR-B protein expression. However, in the uterus PR-B protein levels increased and peaked earlier than PR-A protein levels after eCG treatment. With prolonged exposure to eCG, PR-B protein levels decreased, whereas PR-A protein levels continued to increase. Furthermore, subsequent treatment with human (h)CG decreased the levels of PR protein isoforms in both tissues in parallel with increased endogenous serum progesterone levels. To further elucidate whether progesterone regulates PR protein isoforms, we demonstrated that a time-dependent treatment with progesterone (P(4)) decreased the expression of PR protein isoforms in both tissues, whereas decreases in p27, cyclin D(2), and proliferating cell nuclear antigen protein levels were observed only in the uterus. To define the potential PR-mediated effects on apoptosis, we demonstrated that the PR antagonist treatment increased the levels of PR protein isoforms, induced mitochondrial-associated apoptosis, and decreased in epidermal growth factor (EGF) and EGF receptor protein expression in both tissues. Interestingly, immunohistochemistry indicated that the induction of apoptosis by PR antagonists was predominant in the epithelium, whereas increase in PR protein expression was observed in stromal cells of both tissues. Taken together, these observations suggest that 1) the tissue-specific and hormonal regulation of PR isoform expression in mouse fallopian tube and uterus, where they are potentially involved in regulation of mitochondrial-mediated apoptosis depending on the cellular compartment; and 2) a possible interaction between functional PR protein and growth factor signaling may have a coordinated role for regulating apoptotic process in both tissues in vivo.
机译：孕酮及其与核孕激素受体（PR）的相互作用PR-A和PR-B在所有哺乳动物的女性生殖功能调节中起关键作用。然而，我们对体内输卵管和子宫中PR蛋白亚型的调节和可能的细胞功能的认识仍然非常有限。在本研究中，我们发现马绒毛膜促性腺激素（eCG）治疗导致两种同工型的表达随时间增加，在输卵管中达到最大水平48 h。 PR-A蛋白表达的调节与PR-B蛋白表达的调节平行。但是，在子宫内，eCG治疗后PR-B蛋白水平升高并达到峰值，早于PR-A蛋白水平。随着长时间接触eCG，PR-B蛋白水平下降，而PR-A蛋白水平继续上升。此外，随后用人（h）CG进行治疗可降低两个组织中PR蛋白同工型的水平，同时增加内源性血清孕激素水平。为了进一步阐明孕激素是否调节PR蛋白亚型，我们证明了时间依赖性的孕激素治疗（P（4））降低了两个组织中PR蛋白亚型的表达，而p27，cyclin D（2）和增殖性蛋白的表达均降低了。仅在子宫中观察到细胞核抗原蛋白水平。为了确定潜在的PR介导的对细胞凋亡的作用，我们证明了PR拮抗剂治疗可增加PR蛋白同工型的水平，诱导线粒体相关的细胞凋亡，并降低两种组织中表皮生长因子（EGF）和EGF受体蛋白的表达。有趣的是，免疫组织化学表明PR拮抗剂诱导的凋亡在上皮细胞中占主导，而在两种组织的基质细胞中PR蛋白的表达均增加。综上所述，这些观察结果表明：1）小鼠输卵管和子宫中PR同工型表达的组织特异性和激素调节，它们可能根据细胞区室参与线粒体介导的细胞凋亡的调节; 2）功能性PR蛋白与生长因子信号传导之间可能的相互作用可能在体内两个组织中均具有调节细胞凋亡过程的协调作用。

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