Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repairCitation formats

  • External authors:
  • Maria Antsiferova
  • Jennifer E. Klatte
  • Enikö Bodó
  • José L. Jorcano
  • Martin M. Matzuk
  • Sabine Werner
  • Heidi Kögel

Standard

Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair. / Antsiferova, Maria; Klatte, Jennifer E.; Bodó, Enikö; Paus, Ralf; Jorcano, José L.; Matzuk, Martin M.; Werner, Sabine; Kögel, Heidi.

In: Laboratory Investigation, Vol. 89, No. 2, 02.2009, p. 131-141.

Research output: Contribution to journalArticlepeer-review

Harvard

Antsiferova, M, Klatte, JE, Bodó, E, Paus, R, Jorcano, JL, Matzuk, MM, Werner, S & Kögel, H 2009, 'Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair', Laboratory Investigation, vol. 89, no. 2, pp. 131-141. https://doi.org/10.1038/labinvest.2008.120

APA

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. https://doi.org/10.1038/labinvest.2008.120

Vancouver

Antsiferova M, Klatte JE, Bodó E, Paus R, Jorcano JL, Matzuk MM et al. Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair. Laboratory Investigation. 2009 Feb;89(2):131-141. https://doi.org/10.1038/labinvest.2008.120

Author

Antsiferova, Maria ; Klatte, Jennifer E. ; Bodó, Enikö ; Paus, Ralf ; Jorcano, José L. ; Matzuk, Martin M. ; Werner, Sabine ; Kögel, Heidi. / Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair. In: Laboratory Investigation. 2009 ; Vol. 89, No. 2. pp. 131-141.

Bibtex

@article{a686862db911409eb57fc3fd68e5b9e9,
title = "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. {\textcopyright} 2009 USCAP, Inc All rights reserved.",
keywords = "Activin, Dermis, Epidermis, Follistatin, Wound healing",
author = "Maria Antsiferova and Klatte, {Jennifer E.} and Enik{\"o} Bod{\'o} and Ralf Paus and Jorcano, {Jos{\'e} L.} and Matzuk, {Martin M.} and Sabine Werner and Heidi K{\"o}gel",
year = "2009",
month = feb,
doi = "10.1038/labinvest.2008.120",
language = "English",
volume = "89",
pages = "131--141",
journal = "Laboratory Investigation",
issn = "0023-6837",
publisher = "Springer Nature",
number = "2",

}

RIS

TY - JOUR

T1 - Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair

AU - Antsiferova, Maria

AU - Klatte, Jennifer E.

AU - Bodó, Enikö

AU - Paus, Ralf

AU - Jorcano, José L.

AU - Matzuk, Martin M.

AU - Werner, Sabine

AU - Kögel, Heidi

PY - 2009/2

Y1 - 2009/2

N2 - 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. © 2009 USCAP, Inc All rights reserved.

AB - 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. © 2009 USCAP, Inc All rights reserved.

KW - Activin

KW - Dermis

KW - Epidermis

KW - Follistatin

KW - Wound healing

U2 - 10.1038/labinvest.2008.120

DO - 10.1038/labinvest.2008.120

M3 - Article

VL - 89

SP - 131

EP - 141

JO - Laboratory Investigation

JF - Laboratory Investigation

SN - 0023-6837

IS - 2

ER -