矽肺
发病机制
纤维化
微泡
炎症
肺纤维化
品脱1
巨噬细胞
医学
癌症研究
肺
免疫学
化学
小RNA
病理
疾病
内科学
基因
体外
帕金
帕金森病
生物化学
作者
Jiaqi Ban,Fangwei Liu,Qi Zhang,Shuai Chang,Xinning Zeng,Jie Chen
标识
DOI:10.1016/j.toxlet.2022.10.004
摘要
Silicosis is a fibrotic lung disease caused by the inhalation of free crystalline silica. Its pathogenesis is extremely complex and involves a variety of cells. Exosomes emerge as a favorable candidate for communication between cells. LncRNA is a major component transported by exosomes in many inflammatory diseases. However, the role of exosomal lncRNA in the pathogenesis of silicosis is still unclear. In this study, the decreased expression of a novel exosomal lncRNA MSTRG.91634.7 in silicosis patients was identified according to high-throughput sequencing. Then, this macrophage-derived exosomal lncRNA MSTRG.91634.7 could regulate the fibroblast's activation by targeting PINK1 in a co-culture system of THP-1 and MRC-5. Finally, the mouse was exposed to 3 mg/50 μL silica to set up the silicosis model. AAV-ov-Pink1 was intratracheally injected to overexpress PINK1 in mice lungs. Our results suggested that PINK1, the target protein of lncRNA MSTRG.91634.7, participated in restricting the silica-induced lung inflammation and fibrosis in mice.
科研通智能强力驱动
Strongly Powered by AbleSci AI