Involvement of Epithelial and endothelial to mesenchymal transition in tissue remolding of rheumatic diseases

上皮和内皮向间质转化参与风湿性疾病的组织重塑

• 批准号: 23591451
• 负责人: SAITO Kazuyoshi
• 金额: $ 3.33万
• 依托单位: University of Occupational and Environmental Health, Japan
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23591451/
• 关键词: リモデリング抑制; Wnt10; 膠原病

The aim of this study is to elucidate the mechanism of EMT and EndoMT in tissue remolding and fibrosis of rheumatic diseases and to develop a new treatment strategy for rheumatic diseases. We conducted immune-staining of skin,lung and kidney tissue from rheumatic disease including rheumatoid arthritis, systemic sclerosis and vasculitis. As a result, a hyperplasia of myofibroblast was observed at the site of prominent progression of tissue fibrosis and vascular remodeling due to endothelial dell proliferation. Immuno-staining revealed both the myoblast and endothelial cells express Wnt10a, suggesting signaling through Wnt10 might involvement in irreversible remodeling in rheumatic diseases. These provocative findings suggest that the inhibition of EndMT/EMT may be a promising target for clinical therapeutic translation in settings such as tissue remodeling which cause of irreversible organ damage in rheumatic deseases.

本研究旨在阐明EMT和EndoMT在风湿性疾病组织重塑和纤维化中的作用机制，为风湿性疾病的治疗提供新的策略。我们对风湿性疾病（包括类风湿性关节炎、系统性硬化症和血管炎）的皮肤、肺和肾组织进行免疫染色。结果，由于内皮细胞增殖，在组织纤维化和血管重塑显著进展的部位观察到肌成纤维细胞增生。免疫组化显示成肌细胞和内皮细胞均表达Wnt 10a，提示通过Wnt 10的信号传导可能参与风湿性疾病的不可逆重塑。这些挑衅性的研究结果表明，EndMT/EMT的抑制可能是一个有前途的目标，临床治疗翻译的设置，如组织重塑，导致不可逆的器官损伤的风湿性疾病。