Guo Jingdong, Lin Quan, Shao Ying, Rong Li, Zhang Duo
Department of Plastic and Reconstructive Surgery, The First Hospital of Jilin University, 71 Xinmin Avenue, Changchun 130021, People's Republic of China.
Can J Physiol Pharmacol. 2017 Apr;95(4):437-442. doi: 10.1139/cjpp-2016-0248. Epub 2016 Nov 24.
The hypertrophic scar is a medical difficulty of humans, which has caused great pain to patients. Here, we investigated the inhibitory effect of miR-29b on scar formation. The scalded model was established in mice and miR-29b mimics or a negative control was subcutaneously injected into the injury skin. Then various molecular biological experiments were performed to assess the effect of miR-29b on scar formation. According to our present study, first, the results demonstrated that miR-29b was down-regulated in thermal injury tissue and miR-29b treatment could promote wound healing, inhibit scar formation, and alleviate histopathological morphologic alteration in scald tissues. Additionally, miR-29b treatment suppressed collagen deposition and fibrotic gene expression in scar tissues. Finally, we found that miR-29b treatment inhibited the TGF-β1/Smad/CTGF signaling pathway. Taken together, our data suggest that miR-29b treatment has an inhibitory effect against scar formation via inhibition of the TGF-β1/Smad/CTGF signaling pathway and may provide a potential molecular basis for future treatments for hypertrophic scars.
增生性瘢痕是人类面临的医学难题，给患者带来了巨大痛苦。在此，我们研究了miR-29b对瘢痕形成的抑制作用。在小鼠中建立烫伤模型，并将miR-29b模拟物或阴性对照皮下注射到损伤皮肤处。然后进行各种分子生物学实验，以评估miR-29b对瘢痕形成的影响。根据我们目前的研究，首先，结果表明miR-29b在热损伤组织中表达下调，miR-29b治疗可促进伤口愈合、抑制瘢痕形成，并减轻烫伤组织的组织病理学形态改变。此外，miR-29b治疗可抑制瘢痕组织中的胶原蛋白沉积和纤维化基因表达。最后，我们发现miR-29b治疗可抑制TGF-β1/Smad/CTGF信号通路。综上所述，我们的数据表明，miR-29b治疗通过抑制TGF-β1/Smad/CTGF信号通路对瘢痕形成具有抑制作用，并可能为未来增生性瘢痕的治疗提供潜在的分子基础。
