Elucidation of the healing mechanism for developing gene therapy in palatal wounds

腭裂患者在婴儿期手术闭合缺损后，常出现上颌骨发育障碍和牙弓狭窄。这被认为是上颚伤口愈合过程中形成的疤痕的结果。Smad 3是TGF-β信号通路的成员之一，其缺失的小鼠表现出明显的创伤愈合加速作用，在本研究中，我们研究了Smad 3磷酸化的特异性抑制剂在创伤修复中的作用，结果发现，Smad 3磷酸化抑制剂可促进创伤愈合，并下调炎症基因的表达。

Cleft palate patients are often subject to maxillary growth impairment and narrow dental arch after surgical closure of the defect in infancy. This is considered to be a consequence of the scar which is formed during palatal wound healing. Smad3 is one of the members concerned to TGF-b signaling pathway, and its deficient mice showed the notably accelerated wound healing in injured palates.In this study, we investigated the effects of a specific inhibitor of Smad3 phosphorylation in wound repair, and as a result, an accelerated wound closure with down regulation of inflammatory genes was observed.