論文

査読有り
2012年8月

Smad2 Decelerates Re-epithelialization during Gingival Wound Healing

JOURNAL OF DENTAL RESEARCH
  • K. Tomikawa
  • ,
  • T. Yamamoto
  • ,
  • N. Shiomi
  • ,
  • M. Shimoe
  • ,
  • S. Hongo
  • ,
  • K. Yamashiro
  • ,
  • T. Yamaguchi
  • ,
  • H. Maeda
  • ,
  • S. Takashiba

91
8
開始ページ
764
終了ページ
770
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1177/0022034512451449
出版者・発行元
SAGE PUBLICATIONS INC

During periodontal regeneration, inhibition of gingival downgrowth is necessary to promote migration of mesenchymal cells into the defects. Transforming growth factor (TGF)-beta is a pleiotropic cytokine that has numerous cell functions, including regulation of epithelial growth. Recent studies have shown that Smad2, a downstream transcription factor of TGF-beta, plays crucial roles in wound healing in the epithelia. Therefore, we investigated the effects of Smad2 overexpression on re-epithelialization of gingival wounds. Transgenic mice overexpressing smad2 driven by the keratin 14 promoter (k14-smad2) were confirmed to have significant Smad2 phosphorylation in gingival basal epithelia. Punch wounds were made in the palatal gingiva, and wound healing was assessed histologically for 7 days. Re-epithelialization was significantly retarded on day 2, while collagen deposition was enhanced on day 7 in k14-smad2 compared with wild-type mice. Moreover, expression of keratin 16 (K16), an indicator of keratinocyte migration, was significantly inhibited in wound-edge keratinocytes in k14-smad2. The inhibition of K16 coincided with the induction of Smad2 in the corresponding epithelia, while BrdU incorporation was unaffected. These results indicated that Smad2 has inhibitory effects in regulating keratinocyte migration during gingival wound healing. TGF-beta/Smad2 signaling mediating alteration of K16 expression must be tightly regulated during periodontal regeneration.

リンク情報
DOI
https://doi.org/10.1177/0022034512451449
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000306493300007&DestApp=WOS_CPL
ID情報
  • DOI : 10.1177/0022034512451449
  • ISSN : 0022-0345
  • Web of Science ID : WOS:000306493300007

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