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Oxygen tension modulates the effects of TNFα in compressed chondrocytes

Tilwani RK 1 , Vessillier S 2 , Pingguan-Murphy B 3 , Lee DA 1 , Bader DL 4 , Chowdhury TT 5

Affiliations 

  • 1 Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, Mile End Road, London, E1 4NS, UK
  • 2 Biotherapeutics Group, National Institute for Biological Standards and Control, South Mimms, Potters Bar, Hertfordshire, EN6 3QG, UK
  • 3 Department of Biomedical Engineering, Faculty of Engineering, University of Malaya, Kuala Lumpur, 50603, Malaysia
  • 4 Faculty of Health Sciences, Southampton General Hospital, University of Southampton, Southampton, SO16 6YD, UK
  • 5 Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, Mile End Road, London, E1 4NS, UK. t.t.chowdhury@qmul.ac.uk
Inflamm Res, 2017 Jan;66(1):49-58.
PMID: 27658702 DOI: 10.1007/s00011-016-0991-5

Abstract

OBJECTIVE AND DESIGN: Oxygen tension and biomechanical signals are factors that regulate inflammatory mechanisms in chondrocytes. We examined whether low oxygen tension influenced the cells response to TNFα and dynamic compression.

MATERIALS AND METHODS: Chondrocyte/agarose constructs were treated with varying concentrations of TNFα (0.1-100 ng/ml) and cultured at 5 and 21 % oxygen tension for 48 h. In separate experiments, constructs were subjected to dynamic compression (15 %) and treated with TNFα (10 ng/ml) and/or L-NIO (1 mM) at 5 and 21 % oxygen tension using an ex vivo bioreactor for 48 h. Markers for catabolic activity (NO, PGE2) and tissue remodelling (GAG, MMPs) were quantified by biochemical assay. ADAMTS-5 and MMP-13 expression were examined by real-time qPCR. 2-way ANOVA and a post hoc Bonferroni-corrected t test were used to analyse data.

RESULTS: TNFα dose-dependently increased NO, PGE2 and MMP activity (all p 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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