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Updated: Jun 21, 2025

Author Spotlight: Advancements in Cell and Tissue Engineering for Tendon Repair
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Author Spotlight: Advancements in Cell and Tissue Engineering for Tendon Repair

Published on: March 1, 2024

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Oncostatin M promotes osteogenic differentiation of tendon-derived stem cells through the JAK2/STAT3 signalling

Jun Yang1, Xiaolin Chen2, Yueshu Wu1

  • 1Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, PR China.

Journal of Orthopaedic Surgery and Research
|July 16, 2024
PubMed
Abstract

Insights

Oncostatin M (OSM) promotes osteogenic differentiation in tendon-derived stem cells (TDSCs). This process involves the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.

Area of Science:

  • Stem cell biology
  • Bone biology
  • Cell signaling

Background:

  • Oncostatin M (OSM) regulates osteogenic differentiation and heterotopic ossification.
  • The specific role and mechanism of OSM in tendon-derived stem cell (TDSC) osteogenic differentiation remain unelucidated.

Purpose of the Study:

  • To investigate the role of Oncostatin M (OSM) in the osteogenic differentiation of tendon-derived stem cells (TDSCs).
  • To elucidate the underlying molecular mechanism of OSM-mediated osteogenic differentiation in TDSCs.

Main Methods:

  • TDSCs were cultured and induced for osteogenic differentiation.
  • Recombinant OSM was applied, and its effects were assessed with and without Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) inhibitors.
  • Alkaline phosphatase staining, alizarin red staining, Western blotting, and qPCR were used to evaluate differentiation and gene/protein expression.

Main Results:

  • Recombinant OSM significantly promoted early and mid-stage osteogenic differentiation of TDSCs.
  • Inhibition of JAK2 or STAT3 pathways attenuated OSM-induced osteogenic differentiation.
  • OSM treatment upregulated osteogenic marker genes and related proteins, which was reversed by pathway inhibitors.

Conclusions:

  • Oncostatin M (OSM) is a positive regulator of osteogenic differentiation in TDSCs.
  • The JAK2/STAT3 signaling pathway is crucial for mediating the effects of OSM on TDSC osteogenic differentiation.
Keywords:
JAK2/STAT3 signallingOncostatin MOsteogenic differentiationTendon-derived stem cells

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