Exosomal miR-214 from endometrial stromal cells inhibits endometriosis fibrosis

AbstractSTUDY QUESTIONIs it possible to improve fibrosis in endometriosis by microRNA-214 delivery in exosomes?SUMMARY ANSWERUpregulation of miR-214 may inhibit fibrogenesis and its delivery by exosomes derived from ectopic endometrial stromal cells (ESCs), offers an alternative therapeutic approach for endometriosis fibrosis.WHAT IS KNOWN ALREADYFibrosis is the primary pathological feature of endometriosis. MiR-214 plays an important role in fibrotic disease. Connective tissue growth factor (CTGF) is a critical fibrogenic mediator of miR-214. The expression of miR-214 is decreased in ectopic ESCs compared with normal ESCs. miRNAs are a natural cargo of exosomes and these could be exploited as carriers of miRNA in replacement therapy.STUDY DESIGN, SIZE, DURATIONPaired eutopic and ectopic endometrial tissue samples were obtained from 10 women with ovarian endometrioma. ESCs and epithelial cells from both were culturedin vitro. RT-PCR, western blot and immunohistochemistry were used to study the effect of transfection with miR-214 mimics on CTGF expression and fibrogenesis respectively, with and without TGF β stimulation. Exosomes were isolated from ectopic ESCs and Endometrioma tissue was isolated from four patients, dispersed an injected (ip) into nude mice and allowed to implant. The mice were treated with miR-214-enriched exosomes or controls to confirm the effect of inhibiting CTGF overexpression on endometriosis fibrosis.PARTICIPANTS/MATERIALS, SETTING, METHODSThe primar...
Source: Molecular Human Reproduction - Category: Molecular Biology Source Type: research