TNFα and IL-1 induce IL-6 expression in human cardiac fibroblasts: Role of p38 MAP kinase subtypes

Turner, Neil A.; Sinfield, John K.; Porter, Karen E.

doi:10.1016/j.yjmcc.2008.02.009

Cited by 2 publications

(3 citation statements)

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“…The role of p38 in the heart is less clear still. Analysis of p38 subtype expression in mouse heart revealed that p38 is lowly expressed at the mRNA and protein level (similar to p38) [45], although our own studies in human CF from multiple patients suggest somewhat higher expression than p38 [58]. We recently showed that the p38/// inhibitor BIRB-0796 significantly reduced IL-1-induced MMP-1 and MMP-10 expression in human CF;…”

Section: P38 and P38mentioning

confidence: 86%

“…For example, synovial fibroblasts in tissue from rheumatoid arthritis patients expressed p38 and p38, but did not express p38 even though this was observed in macrophages [114]. This is in marked contrast to human CF, in which p38 is the most abundant isoform [58].…”

Section: Future Perspectivementioning

confidence: 86%

“…While IL-1-induced MMP-3 was inhibited by either a p38/ inhibitor (SB203580) or a p38/// inhibitor (BIRB-0796), IL-1-induced MMP-1 and MMP-10 expression was sensitive only to inhibition by BIRB-0796 [59]. As human CF express the ,  and  subtypes of p38 at the mRNA and protein level, but relatively little p38 (NA Turner, unpublished observations and [58]), this suggests roles for p38 in stimulating MMP-3 expression, and for p38 or p38 in stimulating MMP-1 and MMP-10 expression. However, it should be noted that BIRB-0796 is also a potent inhibitor of JNK2 [66].…”

Section: Jnkmentioning

confidence: 99%

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Therapeutic Regulation of Cardiac Fibroblast Function: Targeting stress-activated Protein Kinase Pathways

Turner

2011

Future Cardiol.

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Cardiac fibroblasts are key players in the myocardial remodeling process and respond to myocardial damage or dysfunction by adopting a myofibroblast phenotype and undergoing increased proliferation, migration, secretion of bioactive molecules and turnover of the extracellular matrix. Many of the key cellular responses of the heart to injury or stress are mediated via specific signaling cascades involving the stress-activated protein kinases (SAPKs). The SAPKs comprise the p38 MAPK and c-Jun N-terminal kinase families, both of which have been implicated in promoting myocardial damage and adverse cardiac remodeling. This article focuses on SAPK signaling cascades in the heart, with particular emphasis on their modulatory effects on cardiac fibroblast function, inflammation and fibrosis. It also describes current and future therapeutic strategies for inhibiting SAPKs in the myocardium. Understanding the role of SAPK signaling at the cellular level holds potential for developing novel therapies to ameliorate cardiac dysfunction in man.

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Section: P38 and P38mentioning

confidence: 86%

Section: Future Perspectivementioning

confidence: 86%