Activin A Stimulates Aromatase via the ALK4-Smad Pathway in Endometriosis. (19th October 2016)

• Record Type: Journal Article
• Authors: Zheng, Juan; Qu, Juan; Lu, Pinhong; Hou, Zhen; Cui, Yugui; Mao, Yundong; Qi, Xiaochen; Ji, Hui; Liu, Jiayin
• Other Names: Qiu Limei Academic Editor.
• Is Part Of: BioMed research international. Volume 2016(2016)
• Publication Date: 2016-10-19
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2016/5791510
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Endometriosis is an estrogen-dependent disease. We previously found that the expression of Activin A was upregulated in the peritoneal fluid of patients with endometriosis. The results of the present study indicated that Activin A induced estradiol secretion and P450arom expression in endometrial stromal cells (ESCs) derived from endometriosis patients. The mechanism of estrogenic synthesis was regulated by the Activin-Smad pathway in endometrial lesions. The data showed that the effect of Activin A on ESCs was partially abrogated by pretreatment with an inhibitor of ALK4 (the type I receptor, ActRIB) and Smad4-siRNA. Cumulatively, these data suggest that Activin A promotes the secretion of estradiol from ESCs by increasing the expression of P450arom via the ALK4-Smad pathway. These findings indicate the ALK4-Smad pathway may promote ectopic lesion survival and development.