• activation of prommp-2 by u46619 occurs via involvement of p38mapk-nfκb-mt1mmp signaling pathway in pulmonary artery smooth muscle cells

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    جزئیات بیشتر مقاله
    • تاریخ ارائه: 1392/07/24
    • تاریخ انتشار در تی پی بین: 1392/07/24
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     we investigated the mechanism by which txa2 mimetic, u46619, activates prommp-2 in bovine pulmonary artery smooth muscle cells. our study showed that treatment of the cells with u46619 caused an increase in the expression and subsequently activation of prommp-2 in the cells. pretreatment with p38mapk inhibitor, sb203580; and nf-κb inhibitor, bay11-7082 inhibited the expression and activation of prommp-2 induced by u46619. u46619 also induced increase in mt1-mmp expression, which was inhibited upon pretreatment with sb203580 and bay11-7082. u46619 treatment to the cells stimulated p38mapk activity as well as nf-κb activation by iκb-α phosphorylation, translocation of nf-κbp65 subunit from cytosol to nucleus and subsequently, by increasing its dna-binding activity. induction of nf-κb activation seems to be mediated through ikk, as transfection of cells with either ikkα or ikkβ sirna prevented u46619-induced phosphorylation of iκb-α and nf-κbp65 dna-binding activity. u46619 treatment to the cells also downregulated the timp-2 level. pretreatment of the cells with sb203580 and bay11-7082 did not show any discernible change in timp-2 level by u46619. overall, u46619-induced activation of prommp-2 is mediated via involvement of p38mapk-nfκb-mt1mmp signaling pathway with concomitant downregulation of timp-2 expression in bovine pulmonary artery smooth muscle cells.

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