Delayed wound healing is an urgent clinical issue. Cellular communication involving exosome-borne cargo such as miRNA is a critical mechanism involved in wound healing. This study isolated and identified human adipose tissue-derived exosomes (Exo-ATs). The specific effects of Exo-ATs on keratinocytes and fibroblasts were examined. Enriched miRNAs in Exo-ATs were analyzed, and miR-92a-3p was selected. The transfer of Exo-ATs-derived miR-92a-3p to keratinocytes and fibroblasts was verified. miR-92a-3p binding to LATS2 was examined and the dynamic effects of the miR-92a-3p/LATS2 axis were investigated. In a dorsal skin wound model, the in vivo effects of Exo-ATs on wound healing were examined. Exo-AT incubation increased keratinocytes and fibroblast proliferation, migration, and extracellular matrix (ECM) accumulation. miR-92a-3p, enriched in Exo-ATs, could be transferred to keratinocytes and fibroblasts, resulting in enhanced proliferation, migration, and ECM accumulation. Large tumor suppressor kinase 2 (LATS2) was a direct target of miR-92a-3p. miR-92a-3p inhibitor effects on keratinocytes and fibroblasts could be partially reversed by LATS2 knockdown. In a dorsal skin wound model, Exo-ATs accelerated wound healing through enhanced cell proliferation, collagen deposition, re-epithelialization, and YAP/TAZ activation. In conclusion, Exo-ATs improve skin wound healing by promoting keratinocyte and fibroblast migration and proliferation and collagen production by fibroblast, which could be partially eliminated by miR-92a inhibition through its downstream target LATS2 and the YAP/TAZ signaling.

伤口愈合延迟是一个紧迫的临床问题。涉及外泌体携带的货物（例如 miRNA）的细胞通讯是伤口愈合的关键机制。这项研究分离并鉴定了人类脂肪组织来源的外泌体（Exo-AT）。检查了 Exo-AT 对角质形成细胞和成纤维细胞的具体影响。分析了Exo-AT中富集的miRNA，并选择了miR-92a-3p。验证了 Exo-AT 衍生的 miR-92a-3p 向角质形成细胞和成纤维细胞的转移。检查了 miR-92a-3p 与 LATS2 的结合，并研究了 miR-92a-3p/LATS2 轴的动态效应。在背部皮肤伤口模型中，研究了 Exo-AT 对伤口愈合的体内影响。Exo-AT 孵育可增加角质形成细胞和成纤维细胞的增殖、迁移和细胞外基质 (ECM) 积累。富含 Exo-AT 的 miR-92a-3p 可以转移到角质形成细胞和成纤维细胞，从而增强增殖、迁移和 ECM 积累。大肿瘤抑制激酶 2 (LATS2) 是 miR-92a-3p 的直接靶标。LATS2 敲低可以部分逆转 miR-92a-3p 抑制剂对角质形成细胞和成纤维细胞的作用。在背部皮肤伤口模型中，Exo-AT 通过增强细胞增殖、胶原蛋白沉积、上皮再形成和 YAP/TAZ 激活来加速伤口愈合。总之，Exo-AT 通过促进角质形成细胞和成纤维细胞迁移和增殖以及成纤维细胞产生胶原蛋白来改善皮肤伤口愈合，而 miR-92a 通过其下游靶标 LATS2 和 YAP/TAZ 信号传导抑制可部分消除这种影响。