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Updated: May 30, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Oncostatin M is a novel inhibitor of TGF-β1-induced matricellular protein expression

Rita Sarközi1, Christine Hauser, Susie-Jane Noppert

  • 1Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck, Austria.

American Journal of Physiology. Renal Physiology
|August 6, 2011
PubMed

Insights

Oncostatin M (OSM) may protect kidneys from fibrosis by inhibiting key profibrotic factors like TGF-β1. This cytokine reduces the expression of fibrotic proteins and mediators in human kidney cells, suggesting a therapeutic potential.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Biology

Background:

  • Matricellular proteins are linked to kidney fibrosis and renal disease progression.
  • Understanding mechanisms to inhibit fibrogenesis is crucial for treating kidney diseases.

Purpose of the Study:

  • To investigate the antifibrotic effects of Oncostatin M (OSM) in human proximal tubule cells (PTC).
  • To determine OSM's role in inhibiting profibrotic events induced by transforming growth factor-beta 1 (TGF-β1).

Main Methods:

  • Treatment of human PTC with OSM and/or TGF-β1.
  • Analysis of gene and protein expression, including FoxC2, SPARC, TSP-1, TNC, and CTGF.
  • Assessment of intracellular signaling pathways (Stat1, Stat3, Smad2/3) via phosphorylation.
  • Utilized receptor-blocking molecules to elucidate signaling mechanisms.

Main Results:

  • OSM reduced TGF-β1-induced expression of the epithelial-mesenchymal transition mediator FoxC2.
  • OSM attenuated basal and TGF-β1-induced expression of matricellular proteins (SPARC, TSP-1, TNC, CTGF).
  • OSM induced rapid Stat1/Stat3 phosphorylation and transient Smad2/3 phosphorylation, distinct from TGF-β1 signaling.
  • OSM's inhibition of TGF-β1-induced CTGF mRNA expression was independent of Smad2/3 and potentially mediated by Stat1/Stat3 signaling.

Conclusions:

  • Oncostatin M exhibits antifibrotic properties in human proximal tubule cells.
  • OSM may protect against tubulointerstitial fibrosis through mechanisms involving Stat1/Stat3 signaling, independent of Smad2/3.
  • OSM presents a potential therapeutic strategy for mitigating kidney fibrosis.

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