The effects of thyroid hormone on Beta1 integrin and PDGF-beta beta expression in dermal fibroblasts and keratinocytes during wound healing
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During wound healing, keratinocytes in the epidermis and fibroblasts in the dermis are largely responsible for the formation of granulation tissue and re-epithelialization, two processes that are necessary to regenerate functional tissue. β1 integrins, heterodimeric transmembrane cell surface receptors, are found in both keratinocytes and fibroblasts and their presence is integral for the wound repair process. Studies have shown that several subtypes of β1 integrins are up regulated during cutaneous wound healing. Platelet-derived growth factor-ββ (PDGF-ββ) is small polypeptide that is also essential in the wound repair process, as it has many chemotaxic and mitogenic properties. PDGF-ββ is released by platelets, fibroblasts and keratinocytes during wound healing and studies have demonstrated that its receptors in fibroblasts are up regulated during the wound repair process. The topical application of thyroid hormone has been has been shown to accelerate wound healing in mice, although the mechanism of action is unclear. This study examined whether or not the in vitro application of triiodothyronine (T3) to dermal fibroblasts and primary keratinocytes altered the expression of β1 integrin and PDGF-ββ in these cells. The results of this study suggest that thyroid hormone affects the expression of both β1 integrin and PDGF-ββ in vitro, although the data was not found to be statistically significant. Further research investigating the mechanism by which thyroid hormone accelerates wound healing should be conducted. Specifically, the effect that T3 has on the expression β1 integrin and PDGF-ββ in fibroblasts and keratinocytes in wounds should be examined.
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