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Role of NF‐κB transcription factors in antiinflammatory and proinflammatory actions of mechanical signals

Role of NF‐κB transcription factors in antiinflammatory and proinflammatory actions of mechanical... Objective The mechanisms by which chondrocytes convert biomechanical signals into intracellular biochemical events are not well understood. In this study, we sought to determine the intracellular mechanisms of the magnitude‐dependent actions of mechanical signals. Methods Chondrocytes isolated from rabbit articular cartilage were grown on flexible membranes. Cells were subjected to cyclic tensile strain (CTS) of various magnitudes in the presence or absence of interleukin‐1β (IL‐1β), which was used as a proinflammatory signal for designated time intervals. The regulation of NF‐κB was measured by reverse transcriptase–polymerase chain reaction, electrophoretic mobility shift assay, and immunofluorescence. Results CTS of low magnitudes (4–8% equibiaxial strain) was a potent inhibitor of IL‐1β–dependent NF‐κB nuclear translocation. Cytoplasmic retention of NF‐κB and reduction of its synthesis led to sustained suppression of proinflammatory gene induction. In contrast, proinflammatory signals generated by CTS of high magnitudes (15–18% equibiaxial strain) mimicked the actions of IL‐1β and induced rapid nuclear translocation of NF‐κB subunits p65 and p50. Conclusion Magnitude‐dependent signals of mechanical strain utilize the NF‐κB transcription factors as common elements to abrogate or aggravate proinflammatory responses. Furthermore, the intracellular events induced by mechanical overload are similar to those that are initiated by proinflammatory cytokines in arthritis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arthritis & Rheumatism Wiley

Role of NF‐κB transcription factors in antiinflammatory and proinflammatory actions of mechanical signals

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References (28)

Publisher
Wiley
Copyright
Copyright © 2004 by the American College of Rheumatology
ISSN
0004-3591
eISSN
1529-0131
DOI
10.1002/art.20601
pmid
15529376
Publisher site
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Abstract

Objective The mechanisms by which chondrocytes convert biomechanical signals into intracellular biochemical events are not well understood. In this study, we sought to determine the intracellular mechanisms of the magnitude‐dependent actions of mechanical signals. Methods Chondrocytes isolated from rabbit articular cartilage were grown on flexible membranes. Cells were subjected to cyclic tensile strain (CTS) of various magnitudes in the presence or absence of interleukin‐1β (IL‐1β), which was used as a proinflammatory signal for designated time intervals. The regulation of NF‐κB was measured by reverse transcriptase–polymerase chain reaction, electrophoretic mobility shift assay, and immunofluorescence. Results CTS of low magnitudes (4–8% equibiaxial strain) was a potent inhibitor of IL‐1β–dependent NF‐κB nuclear translocation. Cytoplasmic retention of NF‐κB and reduction of its synthesis led to sustained suppression of proinflammatory gene induction. In contrast, proinflammatory signals generated by CTS of high magnitudes (15–18% equibiaxial strain) mimicked the actions of IL‐1β and induced rapid nuclear translocation of NF‐κB subunits p65 and p50. Conclusion Magnitude‐dependent signals of mechanical strain utilize the NF‐κB transcription factors as common elements to abrogate or aggravate proinflammatory responses. Furthermore, the intracellular events induced by mechanical overload are similar to those that are initiated by proinflammatory cytokines in arthritis.

Journal

Arthritis & Rheumatism – Wiley

Published: Nov 1, 2004

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