The effect of Q‐switched 1064‐nm Nd: YAG laser on skin barrier and collagen synthesis via miR‐663a to regulate TGFβ1/smad3/p38MAPK pathway

Abstract

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.

Amphibian-derived peptide homodimer OA-GL17d promotes skin wound regeneration through the miR-663a/TGF-β1/Smad axis

“…We also found that OA-GL17d treatment and miR-663a inhibition activated the Smad signaling pathway and significantly reversed the effect of miR-663a mimic on the Smad pathway, but no obvious synergistic effect with miR-663a inhibitor was observed, which implied that OA-GL17d activated the Smad signaling pathway by inhibiting the expression of miR-663a. According to a previous study, miR-663a targets TGF-β1 in HaCaT cells [ 19 ], and thus we did not perform double luciferase analysis. Therefore, we speculate that OA-GL17d may act on TGF-β1 through miR-663a to activate the Smad signaling pathway, thereby promoting skin wound healing.…”

“…Compared with the vehicle group, OA-GL17d (50 nM) treatment decreased the expression of miR-663a by 56 ± 2% ( n = 3) ( Figure 5a ), thereby indicating that OA-GL17d significantly inhibited miR-663a expression. Previous research has shown that miR-663a targets TGF-β1 in HaCaT cells [ 19 ]. To explore the effects of miR-663a on TGF-β1 expression, miR-663a mimic and inhibitor were transfected into HaCaT cells.…”

“…However, the role of miRNA in skin wound repair remains poorly understood and the discovery of novel miRNAs may provide a new strategy for wound care and regeneration. Previous study has shown that laser exposure affects the skin barrier and collagen synthesis by modulating transforming growth factor-β1 (TGF-β1) level via the miR-663a/Smad3/p38MAPK signaling pathway [ 19 ]. However, it is not clear whether miR-663a affects skin wound repair.…”

Expression Profiles and Functional Analysis of Plasma Exosomal Circular RNAs in Acute Myocardial Infarction

“…Since circRNAs have more miRNA binding sites as compared to linear miRNA sponges [ 65 , 66 ], the predominant function of miRNA sponges could be to reduce the activity of target miRNAs and increase the complexity of the competing endogenous RNA (ceRNA) network [ 67 , 68 ]. Hsa-miR-423 was previously reported to inhibit cardiomyocyte apoptosis [ 69 ] while hsa-miR-663a has been shown to increase monocyte adhesion and endothelial cell inflammation [ 70 , 71 ]. In addition, hsa-miR-23b can suppress endothelial cell proliferation [ 72 ].…”

Nd: YAG laser activates the TGFBR1‐SMAD4‐Col3a1 axis via miR‐27a‐3p in photoaged rat skin

“…Low fluence and big spot size of Q-switched 1064 nm Nd:YAG laser (1064-QSNYL) treatment is a noninvasive method for skin rejuvenation and melasma. 9,10 Previous study showed that with the fluence of 1.5 J/cm 2 and spot size of 6 mm, 1064-QSNYL treatment upregulates TGF-β1 and SMAD3, and contributes to collagen synthesis. 9 The effect of the 1064-QSNYL treatment on TGBFR1, SMAD4, and miR-27a-3p in skin photoaging remains unclear.…”