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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Mepacrine inhibits matrix metalloproteinases-1 (MMP-1) and MMP-9 activation in human fibroblast-like synoviocytes.

OBJECTIVE: Matrix metalloproteinases (MMP) are enzymes known to be involved in normal physiological and in many pathological conditions. Rheumatic diseases are among the ailments where MMP have been shown to exert detrimental effects. Mepacrine is used alone or in combination with other drugs to treat lupus and other rheumatic diseases. We investigated whether mepacrine's beneficial effects might be due to its influence on MMP. METHODS: Human fibroblast-like synoviocytes were used to study the effect of mepacrine on phorbol myristic acetate (PMA) induced activation of MMP. Western blot, reverse transcription-polymerase chain reaction, and electrophoretic mobility shift assay (EMSA) experiments were used to investigate the effect of mepacrine. RESULTS: Mepacrine selectively inhibited MMP in human fibroblast-like synoviocytes. Mepacrine inhibited MMP-1 as well as MMP-9, but had no effect on MMP-3 at the mRNA level. Possible mechanisms to explain these findings were investigated, and it was found that mepacrine had a strikingly different effect on c-Jun, as opposed to c-Fos activation. While mepacrine treatment alone led to increased concentrations of c-Jun within the nuclear compartment, c-Fos translocation into the nucleus was blocked in synoviocytes treated with mepacrine and stimulated with PMA. Accordingly, EMSA showed reduced AP-1 binding in mepacrine treated synoviocytes. These results imply that the observed effects of mepacrine on immediate early genes resulted in reduced AP-1 binding. That ultimately led to a selective suppression of genes that rely on unhindered assembling of these transcription factors for their activation. CONCLUSION: Selective inhibition of MMP by mepacrine might in part explain the beneficial effects of this drug in the treatment of certain diseases.[1]


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