期刊
TOXICOLOGY
卷 451, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2021.152683
关键词
Silicosis; miR-490-3p; SNHG20; Fibroblast activation
资金
- National Natural Science Foundation of China [81874258]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
Silicosis is a common occupational disease caused by long-term exposure to crystalline silica. Recent studies have shown the important role of miR-490-3p in silica-induced pulmonary fibrosis by regulating TGFBR1 gene. The results suggest that the SNHG20/miR-490-3p/TGFBR1 axis may serve as a new therapeutic target for pulmonary fibrosis.
Silicosis is a universal occupational disease, which is caused by long-term crystalline silica exposure. Recent studies have shown that noncoding RNAs participate in diverse pathological cellular pathways. However, the precise regulation mechanism remains limited in silicosis. Here, we established a silica-induced mouse fibrosis model (all mice received a one-time intratracheal instillation with 50 mg/kg of silica in 0.05 mL sterile saline). MiR-490-3p was significantly downregulated in silica-induced fibrotic mouse lung tissues and TGF-beta 1 treated fibroblasts. Moreover, overexpressed miR-490-3p could relieve silica-induced lung fibrosis in vivo, and prevent the process of fibroblast-to-myofibroblast transition(FMT)in vitro. Mechanistically, TGFBR1 was one of the major target genes of miR-490-3p, and tightly associated with the process of fibroblasts activation. SNHG20, as opposed to miR-490-3p expression, was elevated in TGF-beta 1-treated fibroblast cell lines and contributed to decreased levels of miR-490-3p. Taken together, these data indicated that miR-490-3p plays a key role in silica-induced pulmonary fibrosis. Our results suggested that SNHG20/miR-490-3p/TGFBR1 axis may provide a new treatment target of pulmonary fibrosis.
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