Heat shock protein 90 regulates IκB kinase complex and NF-κB activation in angiotensin II-induced cardiac cell hypertrophy

Lee, Kyung Hye; Jang, Yangsoo; Chung, Ji Hyung

doi:10.3858/emm.2010.42.10.069

Cited by 35 publications

(24 citation statements)

References 39 publications

(45 reference statements)

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“…The most abundant form of NF-κB is the heterodimer composed of p50 and p65 38, 39 . In the present study, the protein expressions of p50, p65, and p-p65 in the kidney of rats were measured to investigate the underlying mechanism of H 2 S on the cytokine regulation.…”

Section: Resultsmentioning

confidence: 99%

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Luo

Wang

et al. 2017

Sci Rep

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Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H2S significantly improved the kidney structure and function of CRF rats. We found that H2S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H2S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H2S significantly abolished the phosphorylation of extracellular signal-regulated protein kinase 1/2, c-Jun N-terminal kinase, and p38 in the kidney of CRF rats. Furthermore, H2S decreased the expression levels of tumor necrosis factor-α, interleukin (IL)-6, IL-10, and monocyte chemoattractant protein-1, as well as the protein levels of p50, p65, and p-p65 in the kidney of CRF rats. In conclusion, H2S could ameliorate adenine-induced CRF in rats by inhibiting apoptosis and inflammation through ROS/mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways.

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Section: Resultsmentioning

confidence: 99%

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Luo

Wang

et al. 2017

Sci Rep

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“…In endothelial cells, enhanced affinity of HSP90 and IKK leads to increased NF-jB activation and cellular dysfunction [47]. Furthermore, in cardiac cells the HSP90 inhibitor GA prevented HSP90-IKK complex formation, leading to increased IKKa/b degradation [48]. Treatment with HSP90 inhibitors in bladder cancer cells has also been shown to down-regulate expression of IKK, which resulted in reduced NF-jB activity [49].…”

Section: Discussionmentioning

confidence: 99%

“…In a recent study, treatment with 17-DMAG for 24 h reduced IjB phosphorylation in cancer cells [19]. IjB phosphorylation was also reduced in cardiac cells treated with GA and this decrease was attributed to the reduction in IKK expression, and not due to a direct interaction between HSP90 and IjB [48]. In addition, a 4-h treatment with 17-DMAG prevented IjBa from being phosphorylated in IL-6/IFN-c-activated human vascular smooth muscle cells [50].…”

Section: Discussionmentioning

confidence: 99%

HSP90 inhibition by 17-DMAG reduces inflammation in J774 macrophages through suppression of Akt and nuclear factor-κB pathways

et al. 2012

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“…NF‐κB is recognized as a key transcription factor mediating cardiac hypertrophy . The inhibitor of IκB kinase (IKK) complex (IKKα, IKKβ and IKKγ) contributes to the phosphorylation of IκB under stimulation . AKAP‐Lbc promotes the activation of anchored IKKβ, which in turn results in the phosphorylation and degradation of IκB and activation of NF‐κB.…”

Section: Cardiac Hypertrophymentioning

confidence: 99%

Cardiac function modulation depends on the A‐kinase anchoring protein complex

Zhu

Jiang

Zheng

et al. 2019

J Cellular Molecular Medi

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The A‐kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates. Over the decades, more than 70 different AKAPs have been discovered. Accumulative evidence indicates that AKAPs play crucial roles in the functional regulation of cardiac diseases, including cardiac hypertrophy, myofibre contractility dysfunction and arrhythmias. By anchoring different partner proteins (PKA, PKC, PKD and LTCCs), AKAPs take part in different regulatory pathways to function as regulators in the heart, and a damaged structure can influence the activities of these complexes. In this review, we highlight recent advances in AKAP‐associated protein complexes, focusing on local signalling events that are perturbed in cardiac diseases and their roles in interacting with ion channels and their regulatory molecules. These new findings suggest that AKAPs might have potential therapeutic value in patients with cardiac diseases, particularly malignant rhythm.

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Heat shock protein 90 regulates IκB kinase complex and NF-κB activation in angiotensin II-induced cardiac cell hypertrophy

Cited by 35 publications

References 39 publications

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

HSP90 inhibition by 17-DMAG reduces inflammation in J774 macrophages through suppression of Akt and nuclear factor-κB pathways

Cardiac function modulation depends on the A‐kinase anchoring protein complex

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