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Avocado/soya unsaponifiables enhance the expression of transforming growth factor β1 and β2 in cultured articular chondrocytes

Avocado/soya unsaponifiables enhance the expression of transforming growth factor β1 and β2 in... Objective Avocado and soya unsaponifiables (ASU) have been reported to exert beneficial effects in the treatment of periodontal and osteoarticular diseases. They are supposed to stimulate deposition and repair of extracellular matrix components, but the mechanisms underlying their action are not well understood. In view of the repair potential of osteoarthritic (OA) cartilage and the role that the transforming growth factor β (TGFβ) system could play in that process, we carried out in vitro studies to determine the mechanism of action of ASU on articular chondrocytes that may account for the beneficial effects on cartilage metabolism. Methods Cultured bovine articular chondrocytes were treated with various concentrations of ASU, and the expression of both TGFβ isoforms, 1 and 2, and their receptors (TGFβRI and TGFβRII) was determined by Northern blot and reverse transcriptase–polymerase chain reaction. Cell transfection with TGFβ1 promoter constructs was also used to delineate the cis‐acting sequences mediating ASU responsiveness in chondrocytes. The level of plasminogen activator inhibitor 1 (PAI‐1) was also evaluated by Northern blotting and protein radiolabeling. Results The data indicated that ASU stimulate the expression of TGFβ1, TGFβ2, and PAI‐1 by articular chondrocytes. In contrast, the levels of TGFβRI and TGFβRII were not significantly affected by the compound. Treatment of bovine articular chondrocytes transiently transfected with TGFβ1 promoter constructs suggested that the effect on TGFβ1 expression is mediated by the region located between −732 and −1132 bp. Conclusion The results indicate that the ASU‐induced stimulation of matrix synthesis previously reported in cultured articular chondrocytes could be explained by the ability to enhance TGFβ expression in these cells. Further, ASU increase the production of PAI‐1, an effect that could help in blocking the plasmin cascade that leads to metalloprotease activation. These data suggest that the compound has properties that might promote TGFβ‐induced matrix repair mechanisms in articular cartilage. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arthritis & Rheumatism Wiley

Avocado/soya unsaponifiables enhance the expression of transforming growth factor β1 and β2 in cultured articular chondrocytes

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References (61)

Publisher
Wiley
Copyright
Copyright © 1999 by the American College of Rheumatology
ISSN
0004-3591
eISSN
1529-0131
DOI
10.1002/1529-0131(199901)42:1<148::AID-ANR18>3.0.CO;2-U
pmid
9920025
Publisher site
See Article on Publisher Site

Abstract

Objective Avocado and soya unsaponifiables (ASU) have been reported to exert beneficial effects in the treatment of periodontal and osteoarticular diseases. They are supposed to stimulate deposition and repair of extracellular matrix components, but the mechanisms underlying their action are not well understood. In view of the repair potential of osteoarthritic (OA) cartilage and the role that the transforming growth factor β (TGFβ) system could play in that process, we carried out in vitro studies to determine the mechanism of action of ASU on articular chondrocytes that may account for the beneficial effects on cartilage metabolism. Methods Cultured bovine articular chondrocytes were treated with various concentrations of ASU, and the expression of both TGFβ isoforms, 1 and 2, and their receptors (TGFβRI and TGFβRII) was determined by Northern blot and reverse transcriptase–polymerase chain reaction. Cell transfection with TGFβ1 promoter constructs was also used to delineate the cis‐acting sequences mediating ASU responsiveness in chondrocytes. The level of plasminogen activator inhibitor 1 (PAI‐1) was also evaluated by Northern blotting and protein radiolabeling. Results The data indicated that ASU stimulate the expression of TGFβ1, TGFβ2, and PAI‐1 by articular chondrocytes. In contrast, the levels of TGFβRI and TGFβRII were not significantly affected by the compound. Treatment of bovine articular chondrocytes transiently transfected with TGFβ1 promoter constructs suggested that the effect on TGFβ1 expression is mediated by the region located between −732 and −1132 bp. Conclusion The results indicate that the ASU‐induced stimulation of matrix synthesis previously reported in cultured articular chondrocytes could be explained by the ability to enhance TGFβ expression in these cells. Further, ASU increase the production of PAI‐1, an effect that could help in blocking the plasmin cascade that leads to metalloprotease activation. These data suggest that the compound has properties that might promote TGFβ‐induced matrix repair mechanisms in articular cartilage.

Journal

Arthritis & Rheumatism – Wiley

Published: Jan 1, 1999

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