2007
DOI: 10.1002/dmrr.781
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Rosiglitazone increases matrix production and quenches inflammation: studies in human cells

Abstract: In HF and hSMC, rosiglitazone stimulates the synthesis of matrix components via enhanced TGFbeta expression; when combined with PMA, the resulting PKC activation is mediated by enhanced p38 phosphorylation. On the other hand, rosiglitazone quenches inflammation in both cell types, by counteracting PMA-induced phosphorylation of ERK1/2.

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Cited by 4 publications
(2 citation statements)
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“…Moreover, rosiglitazone did not have any additional effects on KLF5 expression when ERK1/2 was blocked, which suggests that ERK1/2 signaling, at least in part, may be involved in the inhibitory effect of PPAR-γ agonist on Ang II-induced KLF5 expression in VSMCs. In accordance with our study, previous studies have demonstrated that PPAR-γ activation may inhibit Ang II induced ERK1/2 activation in endothelial cells[ 41 , 42 ] and VSMCs [ 43 , 44 ]. Recently, Kim et al has showed the similar result that rosiglitazone might attenuate VSMCs proliferation at least by inhibit ERK1/2 activation and other cell signaling such as, mTOR-p70S6K and -4EBP1 systems[ 45 ].…”
Section: Discussionsupporting
confidence: 93%
“…Moreover, rosiglitazone did not have any additional effects on KLF5 expression when ERK1/2 was blocked, which suggests that ERK1/2 signaling, at least in part, may be involved in the inhibitory effect of PPAR-γ agonist on Ang II-induced KLF5 expression in VSMCs. In accordance with our study, previous studies have demonstrated that PPAR-γ activation may inhibit Ang II induced ERK1/2 activation in endothelial cells[ 41 , 42 ] and VSMCs [ 43 , 44 ]. Recently, Kim et al has showed the similar result that rosiglitazone might attenuate VSMCs proliferation at least by inhibit ERK1/2 activation and other cell signaling such as, mTOR-p70S6K and -4EBP1 systems[ 45 ].…”
Section: Discussionsupporting
confidence: 93%
“…The previous study showed that Cytokine-cytokine receptor interaction regulates immune response and inflammation by activating various signaling pathways, including the MAPK pathway, cytokines such as IL-6 and TNF-α activate the MAPK pathway, leading to increased inflammatory response, which plays an important role in the development of autoimmune diseases and cancers, and that enrichment of this pathway in high-risk groups may imply a stronger inflammatory state or aberrant immune activation 41 , 42 . ECM receptor interaction and Focal adhesion both are associated with extracellular matrix (ECM) and cell adhesion, and previous reports have shown that MAPK signaling is associated with ECM production and degradation, thereby promoting cell migration and proliferation 43 46 , which may be a reflection of the worse prognosis of high-risk groups. Cytoskeletal regulation is critical for cell shape, motility, and division.…”
Section: Discussionmentioning
confidence: 99%