Division of Plastic and Reconstructive Surgery and Critical Care, Department of Surgery, University of Alberta, Edmonton, Alberta, Canada.
Wound Repair Regen. 2012 Mar-Apr;20(2):166-77. doi: 10.1111/j.1524-475X.2012.00773.x.
Transforming growth factor-β inducible early gene (TIEG) is induced by transforming growth factor-β (TGF-β) and acts as the primary response gene in the TGF-β/Smad pathway. TGF-β is a multifunctional growth factor that affects dermal wound healing; however, the mechanism of how TGF-β affects wound healing is still not well understood because of the complexity of its function and signaling pathways. We hypothesize that TIEG may play a role in dermal wound healing, with involvement in wound closure, contraction, and reepithelialization. In this study, we have shown that TIEG1 knockout (TIEG1-/-) mice have a delay in wound closure related to an impairment in wound contraction, granulation tissue formation, collagen synthesis, and reepithelialization. We also found that Smad7 was increased in the wounds and appeared to play a role in this wound healing model in TIEG1-/- mice.
转化生长因子-β诱导早期基因（TIEG）可被转化生长因子-β（TGF-β）诱导，并且作为 TGF-β/Smad 通路中的主要应答基因发挥作用。TGF-β 是一种多功能生长因子，可影响皮肤创伤愈合；然而，由于其功能和信号通路的复杂性，TGF-β 影响创伤愈合的机制仍未被充分理解。我们假设 TIEG 可能在皮肤创伤愈合中发挥作用，参与伤口闭合、收缩和再上皮化。在这项研究中，我们已经表明，TIEG1 敲除（TIEG1-/-）小鼠的伤口闭合延迟与伤口收缩、肉芽组织形成、胶原合成和再上皮化受损有关。我们还发现，Smad7 在伤口中增加，并且似乎在 TIEG1-/-小鼠的这种创伤愈合模型中发挥作用。
