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Updated: Jul 26, 2025
Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
Published on: May 21, 2018
The therapeutic effect of exosomal lncRNA MSTRG.91634.7 on mitochondrial dysfunction during SiO2-induced lung
Jiaqi Ban1, Qi Zhang2, Shuai Chang2
1School of Public Health, the Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang, Guizhou 550025, China; Key Laboratory of Environmental Stress and Chronic Disease Control and Prevention, Ministry of Education, China Medical University, Shenyang, Liaoning 110122, China.
Abstract:
Long-term silica (SiO2) exposure led to irreversible lung fibrosis, in which epithelial-mesenchymal transition (EMT) played an essential role. A novel lncRNA MSTRG.91634.7 in the peripheral exosomes of silicosis patients was reported in our previous study, which could remold the pathological process of silicosis. However, whether its regulatory role on the development of silicosis was related to EMT process is unclear, and its mechanism remains to be further studied. In this study, up-regulating lncRNA MSTRG91634.7 restricted SiO2-activated EMT and restored mitochondrial homeostasis binding to PINK1 in vitro. Moreover, overexpressing PINK1 could inhibit SiO2-activated EMT in pulmonary inflammation and fibrosis in mice. Meanwhile, PINK1 contributed to restoring the SiO2-induced mitochondrial dysfunction in mice lung. Our results revealed that exosomal lncRNA MSTRG.91634.7 from macrophages could restore mitochondrial homeostasis to restrict the SiO2-activated EMT by binding to PINK1 during pulmonary inflammation and fibrosis due to SiO2 exposure.
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