Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair

Maria Antsiferova, Jennifer E. Klatte, Enikö Bodó, Ralf Paus, José L. Jorcano, Martin M. Matzuk, Sabine Werner, Heidi Kögel

Research output: Contribution to journalArticle

13 Scopus citations


Activin is a growth and differentiation factor that controls development and repair of several tissues and organs. Transgenic mice overexpressing activin in the skin were characterized by strongly enhanced wound healing, but also by excessive scarring. In this study, we explored the consequences of targeted activation of activin in the epidermis and hair follicles by generation of mice lacking the activin antagonist follistatin in keratinocytes. We observed enhanced keratinocyte proliferation in the tail epidermis of these animals. After skin injury, an earlier onset of keratinocyte hyperproliferation at the wound edge was observed in the mutant mice, resulting in an enlarged hyperproliferative epithelium. However, granulation tissue formation and scarring were not affected. These results demonstrate that selective activation of activin in the epidermis enhances reepithelialization without affecting the quality of the healed wound.

Original languageEnglish (US)
Pages (from-to)131-141
Number of pages11
JournalLaboratory Investigation
Issue number2
StatePublished - Feb 1 2009



  • Activin
  • Dermis
  • Epidermis
  • Follistatin
  • Wound healing

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

Cite this

Antsiferova, M., Klatte, J. E., Bodó, E., Paus, R., Jorcano, J. L., Matzuk, M. M., Werner, S., & Kögel, H. (2009). Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair. Laboratory Investigation, 89(2), 131-141.