Apoptosis modulation by activin A and follistatin in human endometrial stromal cells

Larissa M. Coutinho, Erica L. Vieira, Cynthia Dela Cruz, Maíra Casalechi, Antonio L. Teixeira, Helen L. Del Puerto, Fernando M. Reis

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Activin A is a growth factor that stimulates decidualization and is abundantly expressed in endometrial proliferative disorders. Nevertheless, whether it directly affects endometrial cell survival is still unknown. This study investigated the effects of activin A on total death and apoptosis rates and on tumor necrosis factor (TNF) release by human endometrial stromal cells (HESC). We performed a controlled prospective in vitro study using primary HESC cultures obtained from healthy reproductive age women (n = 11). Cells were treated with medium alone (control) or activin A (25 ng/mL) or activin A (25 ng/mL) and its antagonist follistatin (250 ng/mL). Apoptosis and total cell death were measured by flow cytometry, while TNF concentrations in culture media were quantified by ELISA. Activin A decreased the percentage of apoptotic/dead cells from 31% to 22% (p < 0.05, paired t-test) and reduced TNF levels in culture medium by 14%, but there was no linear correlation between TNF release and apoptotic rates. Both effects of activin A were reversed by follistatin. These findings indicate that activin A promotes HESC survival, possibly by a TNF-independent pathway. This mechanism may be critical to the actions of activin A upon stromal cell growth and differentiation in physiology and disease.

Original languageEnglish (US)
Pages (from-to)161-165
Number of pages5
JournalGynecological Endocrinology
Issue number2
StatePublished - Feb 1 2016
Externally publishedYes


  • Activin A
  • apoptosis
  • endometrium
  • follistatin

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Obstetrics and Gynecology


Dive into the research topics of 'Apoptosis modulation by activin A and follistatin in human endometrial stromal cells'. Together they form a unique fingerprint.

Cite this