C-reactive protein induces high-mobility group box-1 protein release through activation of p38MAPK in macrophage RAW264.7 cells

Kikuchi, Kôichi; Biswas, Kamal Krishna; Unoshima, Masako; Ito, Takashi; Kikuchi, Kiyoshi; Morimoto, Yoko; Iwata, Masahiro; Tancharoen, Salunya; Oyama, Yoko; Takenouchi, Kazunori; Nawa, Yuko; Arimura, Noboru; Jie, Meng Xiao; Shrestha, Binita; Miura, Naoki; Shimizu, Toshiaki; Mera, Kentaro; Arimura, Shinichiro; Taniguchi, Noboru; Iwasaka, Hideo; Takao, Sonshin; Hashiguchi, Teruto; Maruyama, Ikuro

doi:10.1016/j.carpath.2007.08.006

Cited by 55 publications

(41 citation statements)

References 49 publications

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“…47 Consistent with reported hCRP activation of p38 MAPK and ERK1/2 in endothelial cells and macrophages, 10,48 we found that hCRP increased phosphorylated p38 MAPK and ERK1/2 ex vivo in liver tissues and in vitro in hepatocytes. No activation of JNK by hCRP was observed in rat liver or hepatocytes in our study, which was contrary to the reports that CRP activates the JNK pathway in endothelial cells.…”

Section: Discussionsupporting

confidence: 89%

C-reactive protein impairs hepatic insulin sensitivity and insulin signaling in rats: Role of mitogen-activated protein kinases

et al. 2010

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Plasma C-reactive protein (CRP) concentration is increased in the metabolic syndrome, which consists of a cluster of cardiovascular disease risk factors, including insulin resistance. It is not known, however, whether CRP is merely a marker of accompanying inflammation or whether it contributes causally to insulin resistance. The objective of this study is to investigate the role that CRP may play in the development of insulin resistance. We examined the effect of single-dose intravenous administration of purified human (h)CRP on insulin sensitivity in Sprague-Dawley rats using the euglycemic, hyperinsulinemic clamp technique. hCRP was associated with impaired insulin suppression of endogenous glucose production with no reduction in peripheral tissue glucose uptake, suggesting that hCRP mediated insulin resistance in the liver but not extrahepatic tissues. We further assessed components of the insulin signaling pathway and mitogen-activated protein kinases (MAPKs) in the liver. Liver tissues derived from hCRP-treated rats showed reduced insulin-stimulated insulin receptor substrate (IRS) tyrosine phosphorylation, IRS/phosphatidylinositol 3-kinase (PI3K) association, and Akt phosphorylation, consistent with hCRP-induced impairment of hepatic insulin signaling. Furthermore, hCRP enhanced phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and p38 MAPK as well as IRS-1 Ser 612. Finally, we observed in primary cultured rat hepatocytes that U0126 (a selective inhibitor of MAPK/ERK kinase1/2) corrected hCRP-induced impairment of insulin signaling. Conclusions: hCRP plays an active role in inducing hepatic insulin resistance in the rat, at least in part by activating ERK1/2, with downstream impairment in the insulin signaling pathway. (HEPATOLOGY 2011;53:127-135)

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Section: Discussionsupporting

confidence: 89%

C-reactive protein impairs hepatic insulin sensitivity and insulin signaling in rats: Role of mitogen-activated protein kinases

et al. 2010

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“…[35] The kinetics of HMGB1-or endotoxin-induced TNF-α release is notably different, as HMGB1 induces TNF-α release significantly later than endotoxin, which induces the release of TNF-α in a single peak 2-3 hours after stimulation, whereas HMGB1 induces a biphasic TNF-α response, with the first peak at approximately 3 hours and a second peak 8-10 hours after HMGB1 exposure. Recently, Kawahara et al [36] demonstrated that C-reactive protein, a prominent risk marker for infl ammation, including atherosclerosis, could induce the active release of HMGB1 by macrophages through Fc gamma receptor/p38 mitogen-activated protein kinase (MAPK) signaling pathways.…”

Section: Hmgb1 and Macrophagesmentioning

confidence: 99%

Novel insights for high mobility group box 1 protein-mediated cellular immune response in sepsis:A systemic review

Huang¹,

Yao²,

Zhang³

2012

World Journal of Emergency Medicine

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“…CRP dose dependently induces the production of HMGB1 through the p38 MAPK pathway (Kawahara et al, 2008). In return, HMGB1 triggers the expression of other proinflammatory cytokines and reinforces this way the proinflammatory process (Andersson et al, 2000;Wang et al, 1999).…”

Section: Hmgb1 In Positive Feedback Mechanismmentioning

confidence: 99%

Inflammation and Genetics of Inflammation in Cardiovascular Diseases

Bucová¹

2011

Angina Pectoris

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C-reactive protein induces high-mobility group box-1 protein release through activation of p38MAPK in macrophage RAW264.7 cells

Cited by 55 publications

References 49 publications

C-reactive protein impairs hepatic insulin sensitivity and insulin signaling in rats: Role of mitogen-activated protein kinases

C-reactive protein impairs hepatic insulin sensitivity and insulin signaling in rats: Role of mitogen-activated protein kinases

Novel insights for high mobility group box 1 protein-mediated cellular immune response in sepsis:A systemic review

Inflammation and Genetics of Inflammation in Cardiovascular Diseases

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