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[The inhibition effect of miR-29c on lung fibroblasts transdifferentiation induced by SiO(2)]

J Yang1, Y Zhang2, L Huang3

  • 1Department of Environmental Health and Occupational Medicine, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China.

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi = Zhonghua Laodong Weisheng Zhiyebing Zazhi = Chinese Journal of Industrial Hygiene and Occupational Diseases
|June 11, 2019
PubMed

Insights

MicroRNA-29c (miR-29c) plays a key role in silica-induced lung fibrosis. Inhibiting miR-29c promotes fibroblast to myofibroblast transdifferentiation, suggesting miR-29c as a therapeutic target for lung fibrosis.

Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Cell Biology

Background:

  • Silica dust exposure can induce lung fibrosis.
  • Fibroblast to myofibroblast transdifferentiation is a key process in pulmonary fibrosis.
  • The role of microRNAs in silica-induced lung fibrosis requires further investigation.

Purpose of the Study:

  • To investigate the regulatory effect of miR-29c on the trans-differentiation of pulmonary fibroblasts into myofibroblasts induced by silica dust.
  • To explore miR-29c as a potential therapeutic target for silica-induced lung fibrosis.

Main Methods:

  • Established a silicosis cell model in vitro using rat lung fibroblasts and pulmonary macrophages.
  • Utilized real-time quantitative polymerase chain reaction (RT-qPCR) and Western Blot assays to detect miR-29c and alpha-smooth muscle actin (α-SMA) expression.
  • Created miR-29c overexpression and inhibition cell models via viral transfection to assess α-SMA expression.

Main Results:

  • Silica dust exposure significantly down-regulated miR-29c expression and up-regulated α-SMA mRNA and protein levels in lung fibroblasts.
  • Inhibition of miR-29c led to a significant increase in α-SMA expression.
  • Overexpression of miR-29c significantly decreased α-SMA expression.

Conclusions:

  • miR-29c negatively regulates the trans-differentiation of pulmonary fibroblasts into myofibroblasts.
  • Inhibiting the miR-29c-regulated transdifferentiation process may impede the development of pulmonary fibrosis.
  • miR-29c represents a potential therapeutic target for lung fibrosis induced by silica dust.
Keywords:
Alpha smooth muscle actinMicroRNAMyofibroblastsPulmonary fibroblasts

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