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Loss of expression of miR-335 is implicated in hepatic stellate cell migration and activation

Chao Chen1, Chao-Qun Wu, Zong-Qi Zhang

  • 1Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, No.415 Fengyang Road, Shanghai 200003, China.

Experimental Cell Research
|May 19, 2011
PubMed

Insights

MicroRNA-335 (miR-335) is reduced during hepatic stellate cell (HSC) activation, a key process in liver fibrosis. Restoring miR-335 inhibits HSC migration by downregulating tenascin-C (TNC).

Area of Science:

  • Hepatology
  • Molecular Biology
  • Cell Biology

Background:

  • Hepatic stellate cell (HSC) activation and migration are critical in liver fibrosis.
  • MicroRNAs (miRNAs) regulate HSC functions, but their role in HSC activation and migration is not fully understood.

Purpose of the Study:

  • To investigate the role of microRNAs in HSC activation and migration.
  • To identify specific miRNAs involved in HSC activation and their downstream targets.

Main Methods:

  • Comparative analysis of miRNA expression profiles in quiescent, partially activated, and fully activated HSCs.
  • Gene Ontology (GO) and GO-Map network analysis.
  • Quantitative real-time PCR (qRT-PCR) to validate miR-335 levels.
  • In vitro assays to assess HSC migration and tenascin-C (TNC) expression.

Main Results:

  • MicroRNA-mediated regulation of HSC activation was identified.
  • miR-335 expression was significantly reduced during HSC activation.
  • Restoration of miR-335 inhibited HSC migration and reduced alpha-smooth muscle actin (α-SMA) and collagen type I expression.
  • miR-335 restoration significantly inhibited tenascin-C (TNC) expression, a known promoter of cell migration.

Conclusions:

  • miR-335 plays a crucial role in regulating HSC activation and migration.
  • miR-335 inhibits HSC migration, at least partly, by downregulating TNC expression.
  • Targeting miR-335 may offer a therapeutic strategy for liver fibrosis.

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