Activin A Stimulates Aromatase via the ALK4-Smad Pathway in Endometriosis

Abstract EN

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.