Inhibition by Interleukin-4 of stromelysin expression in human skin fibroblasts: role of PKC

Experimental Cell Research
C PronteraD Rotilio

Abstract

This study explores novel aspects of the interaction between inflammatory mediators and extracellular matrix degradation. Here we have evaluated the effects of a T-cell cytokine interleukin-4 (IL-4) on the expression and activity of a metalloprotease, stromelysin, and its tissue inhibitor (TIMP-1) in human skin fibroblasts. IL-4 strongly decreased stromelysin mRNA levels and stromelysin-producing activity induced by IL-1 beta-treated and untreated cells. Under the same experimental conditions, TIMP-1 mRNA expression was slightly modified. Phorbol ester (PMA), a PKC activator, induced stromelysin gene expression, an effect enhanced by the addition of IL-1 beta. IL-4 was not able to decrease the PMA and PMA + IL1 beta effects. Calphostin, a specific PKC inhibitor, inhibited stromelysin mRNA expression induced by IL-1 beta. Forskolin, a PKA activator, did not modify mRNA levels and was not able to reduce the effect of IL-4 on IL-1 beta-induced stromelysin expression. These data suggest that in human dermal fibroblasts, activation of PKC abolishes the observed IL-4 effect on both basal and IL-1 beta-induced stromelysin gene expression. It therefore appears that lack of PKC activation is a prerequisite for the inhibitory effect of I...Continue Reading

Citations

Apr 8, 2004·Journal of Periodontology·Kosunique JenkinsRuth Carter Borghaei
May 1, 1997·Clinical Immunology and Immunopathology·M Odeh
May 18, 1999·International Journal of Cancer. Journal International Du Cancer·C PronteraD Rotilio
Sep 10, 2004·The Journal of Immunology : Official Journal of the American Association of Immunologists·Céline Van ThemscheYves St-Pierre

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