AI Article Synopsis
- TIEG is a gene activated by TGF-β and is key in the TGF-β/Smad signaling pathway, which impacts dermal wound healing.
- TIEG1 knockout mice showed delayed wound healing due to issues with wound contraction, granulation tissue formation, collagen synthesis, and reepithelialization.
- Increased levels of Smad7 were noted in the wounds of TIEG1-/- mice, suggesting its involvement in the impaired wound healing process.
Article Abstract
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.
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| http://dx.doi.org/10.1111/j.1524-475X.2012.00773.x | DOI Listing |
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