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微小RNA-149通过减弱炎症反应促进无瘢痕伤口愈合。

MicroRNA-149 contributes to scarless wound healing by attenuating inflammatory response.

作者信息

Lang Hongxin, Zhao Feng, Zhang Tao, Liu Xiaoyu, Wang Zhe, Wang Rui, Shi Ping, Pang Xining

机构信息

Department of Stem Cells and Regenerative Medicine, Key Laboratory of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, Liaoning 110013, P.R. China.

Department of Assisted Reproduction, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

出版信息

Mol Med Rep. 2017 Aug;16(2):2156-2162. doi: 10.3892/mmr.2017.6796. Epub 2017 Jun 15.

Abstract

A fibrotic or pathological scar is an undesired consequence of skin wound healing and may trigger a series of problems. An attenuated inflammatory response is a significant characteristic of fetal skin wound healing, which can contribute to the scarless healing of fetal skin. According to deep sequencing data, microRNA‑149 (miR‑149) expression was increased in mid-gestational compared with that in late‑gestational fetal skin keratinocytes. It was demonstrated that overexpression of miR‑149 in HaCaT cells can downregulate the expression of pro‑inflammatory cytokines interleukin (IL)‑1α, IL‑1β, and IL‑6 at basal levels and in inflammatory conditions. Furthermore, miR‑149 was revealed to indirectly accelerate transforming growth factor‑β3 and collagen type III expression in fibroblasts, which are essential cells in extracellular matrix remodeling. In a rat skin wound model, miR‑149 improved the quality of the arrangement of collagen bundles and reduced inflammatory cell infiltration during skin wound healing. These results indicate that miR‑149 may be a potential regulator in improving the quality of skin wound healing.

摘要

纤维化或病理性瘢痕是皮肤伤口愈合的不良后果,可能引发一系列问题。炎症反应减弱是胎儿皮肤伤口愈合的一个显著特征,这有助于胎儿皮肤无瘢痕愈合。根据深度测序数据,与妊娠晚期胎儿皮肤角质形成细胞相比,miR-149在妊娠中期的表达增加。结果表明,在HaCaT细胞中过表达miR-149可在基础水平和炎症条件下下调促炎细胞因子白细胞介素(IL)-1α、IL-1β和IL-6的表达。此外,研究发现miR-149可间接促进成纤维细胞中转化生长因子-β3和III型胶原蛋白的表达,而成纤维细胞是细胞外基质重塑中的关键细胞。在大鼠皮肤伤口模型中,miR-149改善了皮肤伤口愈合过程中胶原束排列的质量,并减少了炎症细胞浸润。这些结果表明,miR-149可能是改善皮肤伤口愈合质量的潜在调节因子。

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