TNF-α and H2O2 induce IL-18 and IL-18Rβ expression in cardiomyocytes via NF-κB activation

Chandrasekar, Bysani; Colston, James T.; Rosa, Sam D. de la; Rao, Perla P; Freeman, Gregory L.

doi:10.1016/s0006-291x(03)00496-0

Cited by 79 publications

(59 citation statements)

References 28 publications

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“…This study expands on several in vitro reports from our group demonstrating the important role of IL-18 in cardiac pathophysiology [14,[21][22][23]. The novel and significant finding of this study is that IL-18 is required for full hypertrophic response in an in vivo murine model of chronic pressure overload.…”

Section: Discussionsupporting

confidence: 73%

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Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Colston

Boylston

Feldman

et al. 2007

Biochemical and Biophysical Research Communications

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Interleukin (IL)-18 is a cardiotropic proinflammatory cytokine chronically elevated in the serum of patients with cardiac hypertrophy (LVH). The purpose of this study was to examine the role of IL-18 in pressure-overload hypertrophy using wild type (WT) and IL-18 −/− (null) mice. Adult male C57Bl/ 6 mice underwent transaortic constriction (TAC) for 7 days or sham surgery. Heart weight/body weight ratios showed blunted hypertrophy in IL-18 null TAC mice compared to WT TAC animals. Microarray analyses indicated differential expression of hypertrophy-related genes in WT versus IL-18 nulls. Northern, Western, and EMSA analyses showed Akt and GATA4 were increased in WT but unchanged in IL-18 null mice. Our results demonstrate blunted hypertrophy with reduced expression of contractile-, hypertrophy-, and remodeling-associated genes following pressure overload in IL-18 null mice, and suggest that IL-18 plays a critical role in the hypertrophic response.

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Section: Discussionsupporting

confidence: 73%

“…Northern Blot Analysis, Western blot analysis, and electrophoretic mobility shift assay (EMSA) were carried out as described [14,[21][22][23].…”

Section: Northern Blot Analysis Western Blot Analysis and Electrophmentioning

confidence: 99%

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Colston

Boylston

Feldman

et al. 2007

Biochemical and Biophysical Research Communications

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“…Macrophage-derived TNF-α contributes to insulin resistance and development of hepatic steatosis in diet-induced obesity [37] . It was also reported that either IFN-γ or TNF-α up-regulates gene expression or posttranslational processing of IL-18 in several tissue cell types [15,38,39] , indicating that IL-18 may contribute to the development of insulin resistance-related NAFLD via a complex cytokine network of IL-18 and many other cytokines such as TNF-α, IFN-γ and IL-1β.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Wang¹,

Wang²,

Liu³

et al. 2008

WJG

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AIM:To investigate the effects of rosiglitazone (RGZ) on expression of interleukin-18 (IL-18) and caspase-1 in liver of non-alcoholic fatty liver disease (NAFLD) rats. METHODS: Twenty-eight Sprague-Dawley (SD) rats were randomly divided into control, NAFLD, and RGZ treated NAFLD groups. A NAFLD rat model of NAFLD was established by feeding the animals with a high-fat diet for 12 wk. The NAFLD animals were treated with RGZ or vehicle for the last 4 wk (week 9-12) and then sacrificed to obtain liver tissues. Histological changes were analyzed with HE, oil red O and Masson's trichrome staining. Expressions of IL-18 and caspase-1 were detected using immunohistochemical staining and semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: The expression levels of both IL-18 and caspase-1 were higher in the liver of NAFLD group than in the control group. Steatosis, inflammation and fibrosis, found in the liver of NAFLD rats, were significantly improved 4 wk after RGZ treatment. The elevated hepatic IL-18 and caspase-1 expressions in NAFLD group were also significantly attenuated after RGZ treatment. CONCLUSION:RGZ treatment can ameliorate increased hepatic IL-18 production and histological changes in liver of NAFLD rats. The beneficial effects of RGZ on NAFLD may be partly due to its inhibitory effect on hepatic IL-18 production.

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“…Protein Analysis-Isolation of whole cell homogenates, electrophoresis, electroblotting, and Western blot analysis by the ECL chemiluminescence detection system were carried out essentially as described (23,32,33). Anti-human caspase-8 (1C12; number 9746), caspase-3 (number 9662), caspase-9 (number 9502), PARP (number 9542), BID (number 2002), and p65 (number 3034) antibodies were obtained from Cell Signaling Technology (Beverly, MA).…”

Section: Methodsmentioning

confidence: 99%

Activation of Intrinsic and Extrinsic Proapoptotic Signaling Pathways in Interleukin-18-mediated Human Cardiac Endothelial Cell Death

Chandrasekar

Vemula

Surabhi

et al. 2004

Journal of Biological Chemistry

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119

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TNF-α and H2O2 induce IL-18 and IL-18Rβ expression in cardiomyocytes via NF-κB activation

Cited by 79 publications

References 28 publications

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Activation of Intrinsic and Extrinsic Proapoptotic Signaling Pathways in Interleukin-18-mediated Human Cardiac Endothelial Cell Death

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