Down-regulation of Smad3 Accelerates Palatal Wound Repair

作者：Yoneda N; Yasue A^*; Watanabe T; Tanaka E

来源：Journal of Dental Research, 2013, 92(8): 716-720.

DOI：10.1177/0022034513491575

• RNA interference
• palatal wound-healing
• gene delivery systems
• mouse
• TGF-beta1
• targeted gene repair

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.

• 出版日期2013-8