著作: [米田 尚子]/[泰江 章博]/[渡邉 哲平]/[田中 栄二]/Down-regulation of Smad3 Accelerates Palatal Wound Repair./[Journal of Dental Research]
(英) Down-regulation of Smad3 Accelerates Palatal Wound Repair.
(英) Smad3-deficient mice exhibit accelerated re-epithelialization and tissue remodeling during palatal wound repair. In addition, transforming growth factor beta 1 (TGF-1) and other inflammatory factors are down-regulated compared with those in wild-type mice. The aim of this study was to examine whether targeting of Smad3 with small interfering RNA (siRNA) accelerates wound-healing and inhibits wound contraction in palatal mucoperiosteal wounds. An initial histological examination of wound closure in mouse palates treated with Smad3-targeted siRNA vs. a scrambled siRNA found that wound-healing was accelerated when levels of Smad3 were decreased. Furthermore, with real-time PCR, mRNA levels of Smad3, TGF-1, monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-1 (MIP-1) were found to be significantly down-regulated in palatal tissue treated with Smad3-targeted siRNA vs. a control siRNA. Protein and mRNA levels of -smooth-muscle actin (-SMA), type I collagen, and fibronectin were also lower in palates treated with Smad3-targeted siRNA vs. control siRNA. Taken together, these results indicate that down-regulation of Smad3 expression by siRNA can accelerate wound-healing and may inhibit wound contraction. Therefore, siRNA-targeted inhibition of Smad3 may represent a valuable therapeutic tool for palatal mucoperiosteal wound-healing.
Journal of Dental Research([国際歯科研究学会])
|年月日||必須||2013年 5月 21日|