Jinno K, Takahashi T, Tsuchida K, Tanaka E, Moriyama K
Department of Orthodontics and Dentofacial Orthopedics, Graduate School of Oral Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8504, Japan.
J Dent Res. 2009 Aug;88(8):757-61. doi: 10.1177/0022034509341798.
Wound healing is a well-orchestrated complex process leading to the repair of injured tissues. It is suggested that transforming growth factor (TGF)-beta/Smad3 signaling is involved in wound healing. The purpose of this study was to investigate the role of TGF-beta/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-beta1, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha compared with WT mice. Fibrocytes, expressing hematopoietic surface marker and fibroblast products, were recruited and produced alpha-smooth-muscle actin in WT mice, but were not observed in Smad3(-/-) mice. These results suggest that TGF-beta/Smad3 signaling may play an important role in the regulation of palatal wound healing.
伤口愈合是一个精心编排的复杂过程，可导致受损组织的修复。有研究表明，转化生长因子（TGF）-β/Smad3信号通路参与伤口愈合。本研究的目的是探讨TGF-β/Smad3信号通路在Smad3基因缺陷（Smad3(-/-)）小鼠腭部伤口愈合中的作用。组织学检查显示，与野生型（WT）小鼠相比，Smad3(-/-)小鼠的上皮细胞和真皮细胞增殖加速了伤口闭合。与WT小鼠相比，Smad3(-/-)小鼠伤口部位的巨噬细胞/单核细胞浸润减少，同时TGF-β1、单核细胞趋化蛋白-1和巨噬细胞炎性蛋白-1α的产生也减少。在WT小鼠中，表达造血表面标志物和成纤维细胞产物的纤维细胞被募集并产生α-平滑肌肌动蛋白，但在Smad3(-/-)小鼠中未观察到。这些结果表明，TGF-β/Smad3信号通路可能在腭部伤口愈合的调节中起重要作用。
