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The importance of thyroid hormone (TH) in wound healing is not well understood. To gain insight, we evaluated the impact of TH deficiency on wound-healing genes in cultured keratinocytes. By RT-PCR, keratin 6a (K6a) and 16 (K16) gene expression in TH replete cells was 3.8- (P &lt; 0.005) and 1.9-fold (P &lt; 0.05) greater, respectively, than expression in TH-deficient cells. By real-time PCR, TH replete cell expression of K6a, K16, and K17 was greater than in deficient cells: 18- (P &lt; 0.001), 10- (P &lt; 0.001), and 4-fold (P &lt; 0.005), respectively. To examine TH requirement for optimal wound healing, we contrasted TH-deficient vs. ip T(3)-treated mice. Four days after wounding, ip T(3)-treated mice had twice the degree of wound closure as hypothyroid mice (P &lt; 0.001). By RT-PCR, K6a and K17 gene expression from control mouse skin was greater than from hypothyroid mouse skin: 5- (P &lt; 0.001) and 1.7-fold (P &lt; 0.05), respectively. T(3) is necessary for the keratinocyte proliferation required for optimal wound healing. T(3) exerts influence by stimulating expression of the wound-healing keratin genes. Thus, for hypothyroid patients undergoing surgery that cannot be delayed until euthyroidism is achieved, our data support T(3) treatment for the perioperative period.

A Role for Thyroid Hormone in Wound Healing through Keratin Gene Expression