Regulation of cell proliferation in female reproductive tracts

雌二醇组和三苯氧胺组小鼠输卵管和阴道中原癌基因c-jun和c-fos的mRNAs表达水平较高，导致雌性生殖道DNA合成和增殖。在以妊娠依赖性乳腺肿瘤(PDMT)为特征的GR/A小鼠中，PDMT的生长主要受c-jun、c-fos和EG基因活性引起的激素水平的控制。在雌性和雄性小鼠生殖道中，细胞凋亡抑制因子Bcl2的表达在Fas基因翻译之前就已经减少，提示Bcl2直接或间接参与了Fas基因的翻译。雌激素、孕激素、EGF和TGFα在体外对早孕胎盘滋养层细胞的增殖有促进作用，但对蜕膜细胞的增殖作用不明显。免疫组织化学研究表明，雌性大鼠在发情周期和早孕期间，子宫和阴道的孕激素受体(PR)表达受卵巢类固醇激素的调节。PR在大鼠子宫中的出现受内源性雌激素以外的其他因素控制。新生雄性大鼠子宫对类固醇激素的反应，如子宫内膜细胞有丝分裂活性、PR表达和蛋白质合成明显受到影响，这是导致这些动物蜕膜反应降低的原因。

The unterus and vagina of ovarimized mice expressed higher levels of proto-oncogene mRNA,c-jun and c-fos mRNAs, by estradiol and tamoxifen, resulting in DNA synthesis and proliferation of female genital tracts. n the GR/A mouse which is characterized by the development of pregnancy-dependent mammary tumors (PDMT), growth of PDMT were dominated by hormonal levels resulting from the activity of c-jun, c-fos and EG ganes. In female and male mouse reproductive tracts, a decrease in Bcl-2, suppressor of apoptosis, occurred before the translation of Fas mRNA,suggesting that Bcl-2 directly or indirectly participates in a translation of Fas mRNA.Estrogen, progesterone, EGF and TGFalpha were effective in stimulating the proliferation in vitro of placental trophoblastic cells from early pregnancy, but were ineffective in doing the proliferation of decidual cell.Immunohistochemical investigation demonctrated in female rats that progesterone receptor (PR) expression in the uterus and vagina was regulated by ovarian steroids during the estrous cycles and early pregnancy. The appearance of PR in rat uterus was controlled by factors other than endogenopus estrogen. The uterine response to the steroids, e.g., mitotic activity PR expression and protein synthesis in the endometrial cells, was markedly affected in neonatally androgenized rats, which is responsible for the lowered decidual response in these animals.