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首页> 外文期刊>Endocrinology >Progesterone increases rat neural progenitor cell cycle gene expression and proliferation via extracellularly regulated kinase and progesterone receptor membrane components 1 and 2.
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Progesterone increases rat neural progenitor cell cycle gene expression and proliferation via extracellularly regulated kinase and progesterone receptor membrane components 1 and 2.

机译：孕酮通过细胞外调节的激酶和孕酮受体膜成分1和2增加大鼠神经祖细胞周期基因的表达和增殖。

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摘要

Progesterone receptor (PR) expression and regulation of neural progenitor cell (NPC) proliferation was investigated using NPC derived from adult rat brain. RT-PCR revealed that PRA mRNA was not detected in rat NPCs, whereas membrane-associated PRs, PR membrane components (PGRMCs) 1 and 2, mRNA were expressed. Progesterone-induced increase in 5-bromo-2-deoxyuridine incorporation was confirmed by fluorescent-activated cell sorting analysis, which indicated that progesterone promoted rat NPC exit of G(0)/G(1) phase at 5 h, followed by an increase in S-phase at 6 h and M-phase at 8 h, respectively. Microarray analysis of cell-cycle genes, real-time PCR, and Western blot validation revealed that progesterone increased expression of genes that promote mitosis and decreased expression of genes that repress cell proliferation. Progesterone-induced proliferation was not dependent on conversion to metabolites and was antagonized by the ERK(1/2) inhibitor UO126. Progesterone-induced proliferation was isomer and steroid specific. PGRMC1 small interfering RNA treatment, together with computational structural analysis of progesterone and its isomers, indicated that the proliferative effect of progesterone is mediated by PGRMC1/2. Progesterone mediated NPC proliferation and concomitant regulation of mitotic cell cycle genes via a PGRMC/ERK pathway mechanism is a potential novel therapeutic target for promoting neurogenesis in the mammalian brain.
机译：使用源自成年大鼠脑的NPC研究了孕酮受体（PR）的表达和神经祖细胞（NPC）增殖的调控。 RT-PCR揭示在大鼠NPC中未检测到PRA mRNA，而表达了膜相关PR，PR膜成分（PGRMC）1和2。荧光激活的细胞分选分析证实了孕酮诱导的5-溴-2-脱氧尿苷掺入的增加，这表明孕酮在5 h促进大鼠NPC退出G（0）/ G（1）相，然后增加分别在6小时的S相和8小时的M相中。细胞周期基因的微阵列分析，实时PCR和Western印迹验证显示，孕酮增加了促进有丝分裂的基因的表达，并减少了抑制细胞增殖的基因的表达。孕酮诱导的增殖不依赖于向代谢物的转化，并且被ERK（1/2）抑制剂UO126拮抗。孕酮诱导的增殖是异构体和类固醇特异性的。 PGRMC1小干扰RNA处理，以及孕酮及其异构体的计算结构分析表明，孕激素的增殖作用是由PGRMC1 / 2介导的。孕酮介导的NPC增殖和通过PGRMC / ERK途径机制对有丝分裂细胞周期基因的伴随调节是促进哺乳动物脑神经发生的潜在新治疗靶标。

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