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Published on: June 14, 2016
Inhibition of MMP-9 expression by PPARgamma activators in human bronchial epithelial cells
1Department of Internal Medicine II, University of Ulm, Robert-Koch-Strasse 8, D-89081 Ulm, Germany. martin.hetzel@medizin.uni-ulm.de
Background:
The release of matrix degrading enzymes such as matrix metalloproteinase 9 (MMP-9) from bronchial epithelial cells is critically involved in airway wall remodelling in chronic inflammatory processes of the respiratory system. MMP-9 expression is induced by inflammatory mediators such as tumour necrosis factor (TNF)-alpha, but to date nothing is known about the mechanisms of inhibition of MMP-9 expression in these cells.
Methods:
A study was undertaken to examine whether activators of the nuclear transcription factor peroxisome proliferator activated receptor gamma (PPARgamma) might modulate MMP-9 expression in two different bronchial epithelial cell lines.
Results:
PPARgamma was expressed and was functionally active in NL20 and BEAS cells. Activation of PPARgamma by rosiglitazone or pioglitazone significantly reduced TNF-alpha and PMA induced MMP-9 gelatinolytic activity in a concentration dependent manner in both cell lines, but did not alter the expression of tissue inhibitor of MMPs type 1 (TIMP-1), the local inhibitor of MMP-9. Northern blot analysis revealed a decrease in MMP-9 mRNA expression following treatment with PPARgamma which resulted from the inhibition of NF-kappaB activation in these cells, as determined by transient transfection assays and electromobility shift assays.
Conclusion:
Activation of PPARgamma in human bronchial epithelial cells limits the expression of matrix degrading MMP-9. This might have therapeutic applications in chronic inflammatory processes of the respiratory system.
Insights
Activators of peroxisome proliferator activated receptor gamma (PPARgamma) inhibit matrix metalloproteinase 9 (MMP-9) expression in bronchial cells. This finding suggests potential therapeutic strategies for chronic respiratory inflammatory diseases.
Area of Science:
- Cell Biology
- Molecular Biology
- Respiratory Medicine
Background:
- Matrix metalloproteinase 9 (MMP-9) release from bronchial epithelial cells contributes to airway remodeling in chronic respiratory inflammation.
- Tumor necrosis factor-alpha (TNF-alpha) induces MMP-9 expression, but inhibitory mechanisms remain unclear.
Purpose of the Study:
- To investigate if peroxisome proliferator activated receptor gamma (PPARgamma) activators can modulate MMP-9 expression in bronchial epithelial cells.
- To explore the underlying mechanisms of PPARgamma-mediated MMP-9 inhibition.
Main Methods:
- Utilized two human bronchial epithelial cell lines (NL20 and BEAS).
- Administered PPARgamma activators (rosiglitazone, pioglitazone) to assess effects on MMP-9 activity and mRNA levels.
- Assessed NF-kappaB activation using transient transfection and electromobility shift assays.
Main Results:
- PPARgamma was expressed and functional in both cell lines.
- PPARgamma activation significantly reduced TNF-alpha and PMA-induced MMP-9 activity and mRNA in a dose-dependent manner.
- MMP-9 inhibition by PPARgamma was linked to the suppression of NF-kappaB activation, without affecting TIMP-1 expression.
Conclusions:
- PPARgamma activation effectively limits MMP-9 expression in human bronchial epithelial cells.
- This mechanism holds potential for therapeutic interventions in chronic inflammatory respiratory conditions.
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