Abstract
BackgroundSkin grafting with the preservation of denatured dermis is a novel strategy for the treatment of burn-injured skin. Denatured dermis has the ability to restore to the morphology and function of normal skin, but the underlying molecular mechanism is elusive. MicroRNAs (miRNA) are small noncoding RNAs and regulate normal physiology as well as disease development. In this study, we assessed the potential role of miRNA-23b (miR-23b) in the regulation of cell proliferation and migration of heat-denatured fibroblasts and identified the underlying mechanism.MethodsThe expression of miR-23b in denatured dermis and heat-denatured fibroblasts was detected by quantitative real-time polymerase chain reaction (RT-PCR). The effects of miR-23b on cell proliferation and migration of heat-denatured fibroblasts were assessed by transient transfection of miR-23b mimics and inhibitor. The target gene of miR-23b and the downstream pathway were further investigated.ResultsmiR-23b was downregulated in denatured dermis and heat-denatured fibroblasts. Downregulation of miR-23b dramatically promoted the proliferation and migration of heat-denatured fibroblasts. Subsequent analyses demonstrated that Smad3 was a direct and functional target of miR-23b in heat-denatured fibroblasts, which was validated by the dual luciferase reporter assay. Moreover, immunohistochemistry analysis showed that denatured dermis from rats displayed enhanced staining of Smad3. In addition, miR-23b modulated denatured dermis by activating the Notch1 and TGF-β signaling pathways.ConclusionsOur findings suggest that downregulation of miR-23b contributes to the recovery of denatured dermis, which may be valuable for treatment of skin burns.
Highlights
Wound healing is a dynamic process characterized by various cellular and physiologic events, including acute and chronic inflammation, re-epithelialization and restoration of the underlying connective tissue
The expression of miR-23b in denatured dermis and heat-denatured fibroblasts was detected by quantitative real-time polymerase chain reaction (RT-PCR)
Subsequent analyses demonstrated that Smad3 was a direct and functional target of miR-23b in heat-denatured fibroblasts, which was validated by the dual luciferase reporter assay
Summary
Wound healing is a dynamic process characterized by various cellular and physiologic events, including acute and chronic inflammation, re-epithelialization and restoration of the underlying connective tissue. Denatured dermis plays an essential role in wound healing and preservation of denatured dermis may be an effective treatment for skin burns to attenuate scar formation and restore normal appearance. It is widely accepted that large sheets of split-thickness autologous skin grafting with the preservation of denatured dermis may be the optimal choice for the management of deep partial-thickness burns [2]. Autologous skin grafting on deep partial-thickness burns, where the depth of retained denatured dermis is 0.10 mm, may help regenerate dermal function and alleviate scar formation [4]. Denatured dermis has the ability to restore to the morphology and function of normal skin, but the underlying molecular mechanism is elusive. We assessed the potential role of miRNA-23b (miR-23b) in the regulation of cell proliferation and migration of heat-denatured fibroblasts and identified the underlying mechanism
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