論文

査読有り 筆頭著者
2008年7月

Neurotrophic regulation of epidermal dedifferentiation during wound healing and limb regeneration in the axolotl (Ambystoma mexicanum)

DEVELOPMENTAL BIOLOGY
  • A. Satoh
  • ,
  • G. M. C. Graham
  • ,
  • S. V. Bryant
  • ,
  • D. M. Gardiner

319
2
開始ページ
321
終了ページ
335
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.ydbio.2008.04.030
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Adult urodeles (salamanders) are unique in their ability to regenerate complex organs perfectly. The recently developed Accessory Limb Model (ALM) in the axolotl provides an opportunity to identify and characterize the essential signaling events that control the early steps in limb regeneration. The ALM demonstrates that limb regeneration progresses in a stepwise fashion that is dependent on signals from the wound epidermis, nerves and dermal fibroblasts from opposite sides of the limb. When all the signals are present, a limb is formed de novo. The ALM thus provides an opportunity to identify and characterize the signaling pathways that control blastema morphogenesis and limb regeneration. In the present study, we have utilized the ALM to identity the buttonhead-like zinc-finger transcription factor, Sp9, as being involved in the formation of the regeneration epithelium. Sp9 expression is induced in basal keratinocytes of the apical blastema epithelium in a pattern that is comparable to its expression in developing limb buds, and it thus is an important marker for dedifferentiation of the epidermis. Induction of Sp9 expression is nerve-dependent, and we have identified KGF as an endogenous nerve factor that induces expression of Sp9 in the regeneration epithelium. (c) 2008 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.ydbio.2008.04.030
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000257734600015&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.ydbio.2008.04.030
  • ISSN : 0012-1606
  • Web of Science ID : WOS:000257734600015

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