Background: Our previous research found that Q-switched 1064-nm Nd: YAG laser (1064-QSNYL) induces skin collagen synthesis by activating TGFβ1/Smad3/ p38MAPKs pathway. Moreover, a lot of studies shown that MicroRNAs (miRNAs) contribute to regulate collagen synthesis and skin barrier. Therefore, we intend to explore the mechanism of 1064-QSNYL on collagen synthesis and skin barrier through miRNAs. Methods:We predicted the upstream miRNAs of TGFβ1 by bioinformatics databases, and verified them through dual-luciferase reporter genes and Western blotting. The expression of collagen, skin barrier-related protein K10 and filaggrin, TIMP-1, and MMP-2 were detected by RT-qPCR and Western blotting, respectively. Moreover, we detected moisture content, elasticity value, TEWL value, SOD vitality, and hydroxyproline content to evaluate skin barrier of mice. H&E staining to observe the change of dermis thickness and inflammation and infiltration of mice skin. Results:The results shown that TGFβ1 was target gene of miR-663a. Moreover, we found that 1064-QSNYL activated TGFβ1/smad3/p38MAPK pathway by downregulating the expression of miR-663a in HaCaT, HDF cells, and mice, thereby promoting expression of Collagen I, Collagen IV, TIMP-1, K10, and filaggrin and inhibiting MMP-2. Furthermore, 1064-QSNYL contributed to moisture content, elasticity, SOD vitality, and hydroxyproline content via miR-663a to activate TGFβ1/smad3/ p38MAPK pathway. Conclusions:In summary, this study found for the first time that 1064-QSNYL contributed to collagen synthesis and skin repair via miR-663a to regulate TGFβ1/smad3/ p38MAPK pathway, thereby achieving skin rejuvenation.
Background: Dermatosis is a general term for diseases of the skin and skin appendages including scleroderma, psoriasis, bullous disease, atopic dermatitis, basal cell carcinoma, squamous cell carcinoma, and melanoma. These diseases affect millions of individuals globally and are a serious public health concern. However, the pathogenesis of skin diseases is not fully understood, and treatments are not optimal. Yes-associated protein (YAP) is a transcriptional coactivator that plays a role in the regulation of gene transcription and signal transduction. Aims:To study the role of Yes-associated protein in skin diseases. Materials and Methods:The present review summarizes recent advances in our understanding of the role of YAP in skin diseases, current treatments that target YAP, and potential avenues for novel therapies.Results: Abnormal YAP expression has been implicated in occurrence and development of dermatosis. YAP regulates the cell homeostasis, proliferation, differentiation, apoptosis, angiopoiesis, and epithelial-to-mesenchymal transition, among other processes. As well as, it serves as a potential target in many biological processes for treating dermatosis. Conclusions:The effects of YAP on the skin are complex and require multidimensional investigational approaches. YAP functions as an oncoprotein that can promote the occurrence and development of cancer, but there is currently limited information on the therapeutic potential of YAP inhibition for cancer treatment. Additional studies are also needed to clarify the role of YAP in the development and maturation of dermal fibroblasts; skin barrier function, homeostasis, aging, and melanin production; and dermatosis.
Background: Skin photoaging is the damage caused by excessive exposure to ultraviolet (UV) irradiation. We investigated the effect of adenosine triphosphate (ATP) supplementation on UVB-induced photoaging in HaCaT cells and its potential molecular mechanism. Materials and methods: The toxicity of ATP on HaCaT cells was examined by the MTT assay. The effects of ATP supplementation on the viability and apoptosis of HaCaT cells were determined by crystal-violet staining and flow cytometry, respectively. Cellular and mitochondrial ROS were stained using fluorescent dyes. Expression of Bax, B-cell lymphoma (Bcl)-2, sirtuin (SIRT)3, and superoxide dismutase (SOD)2 was measured via western blotting. Results: ATP (1, 2 mM) exerted no toxic effect on the normal growth of HaCaT cells. UVB irradiation caused the apoptosis of HaCaT cells, and ATP supplementation inhibited the apoptosis induced by UVB significantly, as verified by expression of Bax and Bcl-2. UVB exposure resulted in accumulation of cellular and mitochondrial reactive oxygen species (ROS), but ATP supplementation suppressed these increases. Expression of SIRT3 and SOD2 was decreased upon exposure to UVB irradiation but, under ATP supplementation, expression of SIRT3 and SOD2 was reversed, which was consistent with the reduction in ROS level observed in ATP-treated HaCaT cells after exposure to UVB irradiation. Conclusions: ATP supplementation can suppress UVB irradiation-induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2.
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