PDF(Pubmed)
Abstract：
The delay in wound healing caused by chronic wounds or pathological scars is a pressing issue in clinical practice, imposing significant economic and psychological burdens on patients. In particular, with the aging of the population and the increasing incidence of diseases such as diabetes, impaired wound healing is one of the growing health problems. MicroRNA (miRNA) plays a crucial role in wound healing and regulates various biological processes. Our results show that miR-618 was significantly upregulated during the inflammatory phase of wound healing.Subsequently, miR-618 promotes the secretion of pro-inflammatory cytokines and regulates the proliferation and migration of keratinocytes. Mechanistically, miR-618 binds to the target gene-Atp11b and inhibits the PI3K-Akt signaling pathway, inhibiting the epithelial-mesenchymal transition (EMT) of keratinocytes. In addition, the PI3K-Akt signaling pathway induces the enrichment of nuclear miR-618, and miR-618 binds to the promoter of Lin7a to regulate gene transcription. Intradermal injection of miR-618 antagomir around full-thickness wounds in peridermal mice effectively accelerates wound closure compared to control. In conclusion, miR-618 antagomir can be a potential therapeutic agent for wound healing.
摘要：
慢性伤口或病理性疤痕引起的伤口愈合延迟是临床实践中的紧迫问题。给患者带来巨大的经济和心理负担。特别是,随着人口老龄化和糖尿病等疾病发病率的增加，伤口愈合受损是日益严重的健康问题之一。微小RNA(miRNA)在创伤愈合中起着至关重要的作用,并调节多种生物过程。我们的结果显示miR-618在伤口愈合的炎症阶段显著上调。随后，miR-618促进促炎细胞因子的分泌并调节角质形成细胞的增殖和迁移。机械上,miR-618与靶基因Atp11b结合并抑制PI3K-Akt信号通路,抑制角质形成细胞的上皮-间质转化（EMT）。此外,PI3K-Akt信号通路诱导细胞核miR-618的富集，miR-618与Lin7a的启动子结合以调节基因转录。与对照相比,在表皮小鼠的全层伤口周围皮内注射miR-618antagomir有效地加速了伤口闭合。总之,miR-618antagomir可以是伤口愈合的潜在治疗剂。
