Acceleration of Palatal Wound Healing in Smad3-deficient Mice
| Autor: | Eiji Tanaka, Keiji Moriyama, T. Takahashi, Kunihiro Tsuchida, K. Jinno |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Epithelium
Monocytes Andrology Mice Transforming Growth Factor beta Fibrocyte Animals Medicine Smad3 Protein Fibroblast General Dentistry Chemokine CCL2 Cell Proliferation Chemokine CCL3 Mice Knockout Wound Healing integumentary system biology Palate business.industry Chemotaxis Macrophages Monocyte Mouth Mucosa Transforming growth factor beta Fibroblasts Actins Hematopoiesis medicine.anatomical_structure Langerhans Cells Antigens Surface Immunology biology.protein business Wound healing Myofibroblast Signal Transduction Transforming growth factor |
| Zdroj: | Journal of Dental Research. 88:757-761 |
| ISSN: | 1544-0591 0022-0345 |
| DOI: | 10.1177/0022034509341798 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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