Decay-accelerating factor promotes endometrial cells proliferation and motility under ovarian hormone stimulation.
The intent of the study was to explore the elevating expression of decay-accelerating factor(DAF) exerts influence on biological behaviors of endometrial stromal cells except in classical immunology on the basis of bioinformatic statistics and clinical miscarriages findings suggesting its potential role in the establishment of endometrial receptivity. We confirmed that DAF locates on the cellular surface of endometrial epithelium and stroma. By using plasmid transfection to down-regulate DAF expression in primary endometrial stromal cells(ESCs), we discovered that DAF expression in ESCs increases in response to estradiol and progesterone stimulation in dose- and time-dependent manners; moreover, tamoxifen and RU486 stimulations to block estrogen receptors(ERs) and progesterone receptors(PRs) respectively result in reduced DAF mRNA and protein, and it is more obvious to block PRs. Meanwhile, knocked-down DAF in ESCs weakens the proliferation, migration and invasion of endometrial cells. Cell cycle analysis showed knocked-down DAF accumulates cells in S phase and diminishes cells in G0/G1 phase, which substantiates DAF mediates endometrial cells proliferation. In conclusion, DAF is a potential molecule involving in endometrial cellular proliferation and motility to verify up-expressed DAF during the WOI may facilitate endometrial physiobiological behavior changes, which shed light on DAF function and potential role in the endometrial receptivity establishment.
['Wang|Lu|L|', 'Zhang|Wei|W|', 'Guan|Hai-Yun|HY|']
D000328:Adult D018958:CD55 Antigens D002465:Cell Movement D049109:Cell Proliferation D004305:Dose-Response Relationship, Drug D004717:Endometrium D004958:Estradiol D005260:Female D006801:Humans D015735:Mifepristone D011374:Progesterone D017154:Stromal Cells D013629:Tamoxifen
Proliferation Motility Hormone Endometrial receptivity DAF