Abstract:
: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-β1 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-β1-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.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Cheng D,Xu Q,Liu Y,Li G,Sun W,Ma D,Ni Cdoi
10.1016/j.tox.2021.152683subject
Has Abstractpub_date
2021-01-19 00:00:00pages
152683eissn
0300-483Xissn
1879-3185pii
S0300-483X(21)00006-8pub_type
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