Acceleration of Palatal Wound Healing in Smad3-deficient Mice
Acceleration of Palatal Wound Healing in Smad3-deficient Mice
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DOI：
10.1177/0022034509341798
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发表时间：
2009-08-01
影响因子：
7.6
通讯作者：
Moriyama, K.
中科院分区：
文献类型：
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作者：
Jinno, K.;Takahashi, T.;Moriyama, K.
伤口愈合是一个精心安排的复杂过程，导致受伤组织的修复。提示转化生长因子(TGF)- β /Smad3信号参与创面愈合。本研究的目的是探讨tgf - β /Smad3信号在Smad3缺陷（Smad3(-/-)）小鼠腭创面愈合中的作用。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愈合。与WT小鼠相比，Smad3（-/-）小鼠损伤区域的巨噬细胞/单核细胞浸润减少，同时tgf - β 1、单核细胞趋化蛋白-1和巨噬细胞炎症蛋白-1 α的产生减少。在WT小鼠中，表达造血表面标记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（-/-）小鼠中没有观察到。这些结果提示，tgf - β /Smad3信号可能在腭创面愈合的调控中发挥重要作用。
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-beta 1, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1 alpha 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.