The retinol-binding protein receptor STRA6 contributes to the pathogenesis of adenomyosis via Wnt/ß-catenin pathway depression [microRNA]
Adenomyosis is an estrogen-dependent disease in which endometrial glands and stroma are pathologically demonstrated in the myometrium. Despite its prevalence and severity of symptoms, the precise etiology and physiopathology of adenomyosis is not well understood.Vitamin defciency increase in women with adenomyosis. Much less is known about the mechanism of their relationship. We found the retinol-binding protein receptor STRA6 upregulation in uterinespiral arteries from adenomyosis patients. The increased estrogen level promote the STRA6 expression, resulting the depressed Wnt/ß-catenin signaling mediated by FASN/GSK-3ß interaction. Overexpression of STRA6 induced epithelial to mesenchymal transition process. miR-1249-5p achieved its negative function by regulating the target gene through 3' UTR.The depletion of STRA6 in vivo alleviated the pathogenesis of adenomyosis. These results reveal a hitherto undesribed positive feedback loop between estrogen and STRA6 in adenomyosis pathogenesis. Components of vitamin A metabolism network have more complex activities than simply controlling or transferring VA compounds between different cells. Overall design: To investigate the pathway through which estrogen participates in the the pathogenesis of adenomyosis, microRNA sequencing were performed on rabbit samples treated with different concentrations of estrogen.  We then performed gene expression profiling analysis of RNA-seq obtained from 3 concentrations of estrogen.