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Published on: March 24, 2017

MicroRNA-29, a key regulator of collagen expression in systemic sclerosis

Britta Maurer1, Joanna Stanczyk, Astrid Jüngel

  • 1University Hospital Zurich and Zurich Center of Integrative Human Physiology, Zurich, Switzerland.

Arthritis and Rheumatism
|March 5, 2010
PubMed
Abstract

Insights

MicroRNA-29a (miR-29a) is downregulated in systemic sclerosis (SSc), leading to increased collagen production. Restoring miR-29a levels may offer a new therapeutic strategy for SSc.

Area of Science:

  • Molecular Biology
  • Immunology
  • Dermatology

Background:

  • Systemic sclerosis (SSc) is characterized by excessive fibrosis.
  • MicroRNAs (miRNAs) are key posttranscriptional regulators.
  • Profibrotic gene dysregulation is central to SSc pathogenesis.

Purpose of the Study:

  • To investigate the role of specific miRNAs in regulating profibrotic genes in SSc.
  • To determine the expression levels and function of miRNA-29 (miR-29) in SSc.
  • To explore miR-29a as a potential therapeutic target for SSc.

Main Methods:

  • In silico analysis to identify miRNAs targeting collagen genes.
  • TaqMan real-time PCR to quantify miR-29 expression in SSc skin/fibroblasts and a mouse model.
  • Cell transfection with miR-29 precursors/inhibitors and luciferase reporter assays.
  • Stimulation with TGF-beta, PDGF-B, IL-4, and inhibition of signaling pathways.

Main Results:

  • miR-29a was significantly downregulated in SSc fibroblasts and skin compared to controls.
  • miR-29a overexpression reduced collagen mRNA/protein; knockdown increased collagen levels.
  • miR-29a directly regulates collagen gene expression.
  • TGF-beta, PDGF-B, and IL-4 reduced miR-29a levels in normal fibroblasts.
  • Imatinib treatment restored miR-29a levels in vitro and in vivo.

Conclusions:

  • Posttranscriptional regulation of collagens by miR-29a is a novel mechanism in SSc fibrogenesis.
  • miR-29a downregulation contributes to excessive collagen deposition in SSc.
  • miR-29a represents a promising therapeutic target for systemic sclerosis.

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