Hypertrophic scar is a common complication after skin injury. MicroRNAs have been reported related to hypertrophic scar through posttranscriptional control of genes. Hypertrophic scar-derived fibroblast model and mice incision model were used to see the expression of microRNA-494 and whether the level changes of microRNA-494 could affect scar formation. It was found that in hypertrophic scar, the expression of microRNA-494 decreased. However, after over-express microRNA-494 in fibroblasts, the levels of scar related molecules such as Col I, Col III increased. And when suppress the level of microRNA-494 in fibroblasts, the levels of collagen decreased. Moreover, the up-regulation of microRNA-494 led to decreased apoptosis of fibroblasts while the down-regulation of it led to increased apoptosis. Further, it was found that PTEN was one of the downstream targets of microRNA-494. The up-regulation of PTEN led to inactivation of PI3K/AKT pathway and the decreased expression of collagens. In conclusion, we confirmed that microRNA-494 could be a key regulator to suppress hypertrophic scar formation. The suppression of microRNA-494 could eliminate its inhibition effect to PTEN and finally decrease the expression of collagen and inhibit hypertrophic scar formation.

中文翻译：

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MicroRNA-494靶向PTEN并抑制PI3K / AKT途径以减轻肥厚性瘢痕的形成。

肥厚性瘢痕是皮肤损伤后的常见并发症。据报道，通过基因的转录后控制，MicroRNA与肥厚性瘢痕有关。使用增生性瘢痕来源的成纤维细胞模型和小鼠切口模型观察microRNA-494的表达以及microRNA-494的水平变化是否会影响瘢痕形成。发现在肥厚性瘢痕中，microRNA-494的表达降低。但是，在成纤维细胞中过表达microRNA-494后，与疤痕相关的分子（例如Col I，Col III）的水平增加。而当抑制成纤维细胞中microRNA-494的水平时，胶原蛋白的水平下降。此外，microRNA-494的上调导致成纤维细胞凋亡减少，而其下调则导致凋亡增加。进一步，发现PTEN是microRNA-494的下游靶标之一。PTEN的上调导致PI3K / AKT通路失活和胶原蛋白表达降低。总之，我们确认microRNA-494可能是抑制肥大性瘢痕形成的关键调节剂。抑制microRNA-494可以消除其对PTEN的抑制作用，最终降低胶原蛋白的表达并抑制肥厚性瘢痕的形成。