Mechanical load modulates chondrogenesis of human mesenchymal stem cells through the TGF-beta pathway

J Cell Mol Med. 2010 Jun;14(6A):1338-46. doi: 10.1111/j.1582-4934.2009.00780.x. Epub 2009 May 11.

Abstract

This study investigated the effect of mechanical load on human mesenchymal stem cell (hMSC) differentiation under different exogenous transforming growth factor-beta1 (TGF-beta(1)) concentrations (0, 1 or 10 ng/ml).The role of the TGF-beta signalling pathway in this process was also studied. Human MSCs were seeded into fibrin-biodegradable polyurethane scaffolds at a cell density of 5 x 10(6) cells per scaffold and stimulated using our bioreactor. One hour of surface motion superimposed on cyclic compression was applied once a day over seven consecutive days. Scaffolds were analysed for gene expression, DNA content and glycosaminoglycan amount. Addition of TGF-beta(1) in the culture medium was sufficient to induce chondrogenesis of hMSCs. Depending on the TGF-beta(1) concentration of the culture medium, mechanical load stimulated chondrogenesis of hMSCs compared to the unloaded scaffolds, with a much stronger effect on gene expression at lower TGF-beta(1) concentrations. With TGF-beta(1) absent in the culture medium, mechanical load stimulated gene transcripts and protein synthesis of TGF-beta(1) and TGF-beta(3). TGF-beta type I receptor inhibitor LY364947 blocked the up-regulation on TGF-beta(1) and TGF-beta(3) production stimulated by mechanical load, and also blocked the chondrogenesis of hMSCs. Taken together, these findings suggest that mechanical load promotes chondrogenesis of hMSCs through TGF-beta pathway by up-regulating TGF-beta gene expression and protein synthesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Chondrogenesis / drug effects*
  • Chondrogenesis / genetics
  • Culture Media, Conditioned / pharmacology
  • DNA / metabolism
  • Enzyme-Linked Immunosorbent Assay
  • Gene Expression Regulation / drug effects
  • Glycosaminoglycans / metabolism
  • Humans
  • Mesenchymal Stem Cells / drug effects*
  • Mesenchymal Stem Cells / metabolism*
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Protein Serine-Threonine Kinases / metabolism
  • Receptor, Transforming Growth Factor-beta Type I
  • Receptors, Transforming Growth Factor beta / antagonists & inhibitors
  • Receptors, Transforming Growth Factor beta / metabolism
  • Signal Transduction / drug effects*
  • Stress, Mechanical*
  • Tissue Scaffolds
  • Transforming Growth Factor beta1 / pharmacology*
  • Transforming Growth Factor beta3 / pharmacology

Substances

  • Culture Media, Conditioned
  • Glycosaminoglycans
  • Receptors, Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Transforming Growth Factor beta3
  • DNA
  • Protein Serine-Threonine Kinases
  • Receptor, Transforming Growth Factor-beta Type I