ERK activation is required for hydrostatic pressure-induced tensile changes in engineered articular cartilage

G. D. Duraine, K. A. Athanasiou

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

The objective of this study was to identify ERK 1/2 involvement in the changes in compressive and tensile mechanical properties associated with hydrostatic pressure treatment of self-assembled cartilage constructs. In study 1, ERK 1/2 phosphorylation was detected by immunoblot, following application of hydrostatic pressure (1h of static 10MPa) applied at days 10-14 of self-assembly culture. In study 2, ERK 1/2 activation was blocked during hydrostatic pressure application on days 10-14. With pharmacological inhibition of the ERK pathway by the MEK1/ERK inhibitor U0126 during hydrostatic pressure application on days 10-14, the increase in Young's modulus induced by hydrostatic pressure was blocked. Furthermore, this reduction in Young's modulus with U0126 treatment during hydrostatic pressure application corresponded to a decrease in total collagen expression. However, U0126 did not inhibit the increase in aggregate modulus or GAG induced by hydrostatic pressure. These findings demonstrate a link between hydrostatic pressure application, ERK signalling and changes in the biomechanical properties of a tissue-engineered construct.

Original languageEnglish (US)
Pages (from-to)368-374
Number of pages7
JournalJournal of Tissue Engineering and Regenerative Medicine
Volume9
Issue number4
DOIs
StatePublished - Apr 1 2015

Keywords

  • Cartilage
  • Chondrocyte
  • Extracellular signal-regulated kinase 1/2 (ERK 1/2)
  • Hydrostatic pressure
  • Self-assembly
  • Tissue engineering

ASJC Scopus subject areas

  • Biomedical Engineering
  • Medicine (miscellaneous)
  • Biomaterials

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