Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair.

Abstract	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.
Authors	Maria Antsiferova, Jennifer E Klatte, Enikö Bodó, Ralf Paus, José L Jorcano, Martin M Matzuk, Sabine Werner, Heidi Kögel
Journal	Laboratory investigation; a journal of technical methods and pathology (Lab Invest) Vol. 89 Issue 2 Pg. 131-41 (Feb 2009) ISSN: 1530-0307 [Electronic] United States
PMID	19079322 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References	Bmp2 protein, mouse Bone Morphogenetic Protein 2 Follistatin Myostatin RNA, Messenger inhibin beta A subunit Inhibin-beta Subunits Bromodeoxyuridine
Topics	Animals Bone Morphogenetic Protein 2 (genetics, metabolism) Bromodeoxyuridine (metabolism) Cell Proliferation Cells, Cultured Cicatrix, Hypertrophic (metabolism, pathology) Epidermis (metabolism, pathology) Female Follistatin (genetics, metabolism) Gene Expression Granulation Tissue (metabolism, pathology) Homeostasis (physiology) Inhibin-beta Subunits (genetics, metabolism) Keratinocytes (cytology, metabolism) Male Mice Mice, Knockout Mice, Transgenic Myostatin (genetics, metabolism) RNA, Messenger (metabolism) Wound Healing (physiology)

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