Department of Plastic Surgery, The Second Affiliated Hospital of Xi'an Medical College, China; Department of Burns and Cutaneous Surgery, Xijing Hospital, The Fourth Military Medical University, China.
Department of Plastic Surgery, The Second Affiliated Hospital of Xi'an Medical College, China.
Arch Biochem Biophys. 2023 Sep 15;746:109733. doi: 10.1016/j.abb.2023.109733. Epub 2023 Aug 29.
Pathological scarring is the greatest challenge after injury. Exosome from adipose-derived mesenchymal stem cells has been reported effective to improve hypertrophic scar. This study focused on the possible mechanisms during this process. Exosomes from adipose-derived mesenchymal stem cells were extracted first. Hypertrophic scar tissue and paired normal skin tissue were collected from patients. Mice skin incision model and fibroblasts model were established. TGF-β1 was used to stimulate fibroblasts to myofibroblasts transdifferentiation. It was found that exosomes injection could decrease collagen sediment after wound healing. During which, the expression of microRNA-181a decreased. Further, we found that expression of microRNA-181a in scar tissue was higher than in normal skin. Then hypertrophic scar-derived fibroblasts were used for in vitro study. It was found that similar to the use of exosomes, microRNA-181a inhibitor decreased the expression of collagen and α-SMA. While microRNA-181a mimics suppressed the effects of exosomes. During fibroblast to myofibroblast trans-differentiation, level of microRNA-181a well as levels of scar-related molecules also decreased with the use of exosomes and vice versa. SIRT1 was confirmed one of the downstream targets of microRNA-181a. Suppression of SIRT1 led to diminished effects of exosomes in hypertrophic scar derived fibroblasts. In mice skin incision model, injection of SIRT1 inhibitor led to increased collagen synthesis. In conclusion, exosomes from Adipose-derived mesenchymal stem cells are promising to antagonize scarring through the regulation of microRNA-181a/SIRT1 axis.
病理性瘢痕是创伤后最大的挑战。脂肪间充质干细胞来源的外泌体已被报道可有效改善增生性瘢痕。本研究主要关注这一过程中的可能机制。首先提取脂肪间充质干细胞来源的外泌体。从患者中收集增生性瘢痕组织和配对正常皮肤组织。建立小鼠皮肤切口模型和成纤维细胞模型。用 TGF-β1 刺激成纤维细胞向肌成纤维细胞转分化。结果发现,外泌体注射可减少伤口愈合后的胶原沉淀。在此过程中,miR-181a 的表达降低。进一步发现,瘢痕组织中 miR-181a 的表达高于正常皮肤。然后用增生性瘢痕来源的成纤维细胞进行体外研究。结果发现,与外泌体的使用相似,miR-181a 抑制剂降低了胶原和α-SMA 的表达。而 miR-181a 模拟物抑制了外泌体的作用。在成纤维细胞向肌成纤维细胞转分化过程中,miR-181a 的水平以及与瘢痕相关的分子水平也随着外泌体的使用而降低,反之亦然。SIRT1 被证实是 miR-181a 的下游靶标之一。沉默 SIRT1 导致外泌体在增生性瘢痕成纤维细胞中的作用减弱。在小鼠皮肤切口模型中,SIRT1 抑制剂的注射导致胶原合成增加。总之,脂肪间充质干细胞来源的外泌体通过调节 miR-181a/SIRT1 轴有望拮抗瘢痕形成。