Acceleration of palatal wound healing in Smad3-deficient mice

K. Jinno, T. Takahashi, Kunihiro Tsuchida, E. Tanaka, K. Moriyama

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Wound healing is a well-orchestrated complex process leading to the repair of injured tissues. It is suggested that transforming growth factor (TGF)-β/ Smad3 signaling is involved in wound healing. The purpose of this study was to investigate the role of TGF-β/Smad3 signaling in palatal wound healing in Smad3-deficient (Smad3-/-) mice. Histological examination showed that wound closure was accelerated by the proliferation of epithelium and dermal cells in Smad3-/- mice compared with wild-type (WT) mice. Macrophage/monocyte infiltration at wounded regions in Smad3-/- mice was decreased in parallel with the diminished production of TGF-β1, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1α compared with WT mice. Fibrocytes, expressing hematopoietic surface marker and fibroblast products, were recruited and produced α-smooth-muscle actin in WT mice, but were not observed in Smad3-/- mice. These results suggest that TGF-β/Smad3 signaling may play an important role in the regulation of palatal wound healing.

Original languageEnglish
Pages (from-to)757-761
Number of pages5
JournalJournal of Dental Research
Volume88
Issue number8
DOIs
Publication statusPublished - 01-08-2009

All Science Journal Classification (ASJC) codes

  • Dentistry(all)

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