MiR-411–3p alleviates Silica-induced pulmonary fibrosis by regulating Smurf2/TGF-β signaling

Gao, Xuemin; Xu, Hong; Xu, Danfeng; Li, Shumin; Wei, Zhongqiu; Cai, Wenchen; Mao, Na; Jin, Fuyu; Li, Yaqian; Li, Tian; Xue, Yu; Liu, Heliang; Fang, Yang

doi:10.1016/j.yexcr.2020.111878

Cited by 19 publications

(21 citation statements)

References 31 publications

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“…In a previous study, we have demonstrated that miR-411-3p inhibits lung fibroblast viability and migration induced by Smurf2/TGF-b1 signaling. 31 Taken together, these findings provide strong support for the notion of miRNA targeting as a therapeutic strategy in the treatment of pulmonary silicosis.…”

Section: Discussionmentioning

confidence: 55%

“…Mice were divided into four groups: (1) control, (2) silica, 32,33 (3) silica plus agomir-Negative control (NC), and (4) silica plus agomir miR411-3P (n = 6 animals per group). 31,34 In these studies, pulmonary silicosis was induced by administering a one-time dose of SiO 2 dust into the posterior oropharynx. 35 Silica dust (5-mm silica particles, S5631, Sigma-Aldrich) was administered at a concentration of 100 mg/kg.…”

Section: Animal Experimentsmentioning

confidence: 99%

“…One week after silica dust administration, 0.05 mL control (agomir-NC) or agomir miR411-3P (5 nmol/mL, RiboBio, Guangzhou,China) was administered by tail vein injection. 31 Animals were sacrificed at day 14 after silica administration, and harvested lungs were then stored at À80 C for subsequent analysis.…”

Section: Animal Experimentsmentioning

confidence: 99%

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Pulmonary Silicosis Alters MicroRNA Expression in Rat Lung and miR-411-3p Exerts Anti-fibrotic Effects by Inhibiting MRTF-A/SRF Signaling

Gao

et al. 2020

Molecular Therapy - Nucleic Acids

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To identify potential therapeutic targets for pulmonary fibrosis induced by silica, we studied the effects of this disease on the expression of microRNAs (miRNAs) in the lung. Rattus norvegicus pulmonary silicosis models were used in conjunction with high-throughput screening of lung specimens to compare the expression of miRNAs in control and pulmonary silicosis tissues. A total of 70 miRNAs were found to be differentially expressed between control and pulmonary silicosis tissues. This included 41 miRNAs that were upregulated and 29 that were downregulated relative to controls. Among them, miR-292-5p, miR-155-3p, miR-1193-3p, miR-411-3p, miR-370-3p, and miR-409a-5p were found to be similarly altered in rat lung and transforming growth factor (TGF)-b1-induced cultured fibroblasts. Using miRNA mimics and inhibitors, we found that miR-1193-3p, miR-411-3p, and miR-370-3p exhibited potent anti-fibrotic effects, while miR-292-5p demonstrated profibrotic effects in TGF-b1-stimulated lung fibroblasts. Moreover, we also found that miR-411-3p effectively reduced pulmonary silicosis in the mouse lung by regulating Mrtfa expression, as demonstrated using biochemical and histological assays. In conclusion, our findings indicate that miRNA expression is perturbed in pulmonary silicosis and suggest that therapeutic interventions targeting specific miRNAs might be effective in the treatment of this occupational disease.

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Section: Discussionmentioning

confidence: 55%

Section: Animal Experimentsmentioning

confidence: 99%

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Pulmonary Silicosis Alters MicroRNA Expression in Rat Lung and miR-411-3p Exerts Anti-fibrotic Effects by Inhibiting MRTF-A/SRF Signaling

Gao

et al. 2020

Molecular Therapy - Nucleic Acids

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“…2,3 Such factors facilitate the activation and proliferation of lung fibroblasts, which further secrete extracellular matrix, leading to pulmonary fibrosis. [4][5][6] Therefore, targeting lung fibroblasts may be a feasible strategy for developing new antifibrotic drugs for silicosis.…”

Section: Introductionmentioning

confidence: 99%

“…Silica particles can activate alveolar macrophages and damage epithelial cells to release a large number of pro‐fibrotic factors (TGF‐β1, CTGF, PDGF, etc) 2,3 . Such factors facilitate the activation and proliferation of lung fibroblasts, which further secrete extracellular matrix, leading to pulmonary fibrosis 4‐6 . Therefore, targeting lung fibroblasts may be a feasible strategy for developing new antifibrotic drugs for silicosis.…”

Section: Introductionmentioning

confidence: 99%