Heat shock treatment protects against angiotensin II–induced hypertension and inflammation in aorta

Chen, Yu; Ross, B.; Currie, R. William

doi:10.1379/csc-1r.1

Cited by 23 publications

(22 citation statements)

References 45 publications

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“…HS has been shown to inhibit ANG II-induced hypertension and inflammation in the heart and aorta (23,34). This suggests the presence of cross talk between HS and RAS.…”

Section: Discussionmentioning

confidence: 96%

“…We and others (1,4) have reported that the activation of ANG II is responsible for endothelial dysfunction in insulin resistance. Earlier, HS has been shown to suppress ANG II-induced hypertension and inflammation, but there are no reports suggesting a beneficial role of HS on the ANG-(1-7) pathway of RAS (23). Therefore, we determined vasodilator responses to ANG-(1-7) in insulin resistance condition.…”

Section: Hs Treatment Improves Ang-(1-7)-induced Vasodilator Responsesmentioning

confidence: 98%

“…This interesting observation can explain the decreased expression of HSP72, SIRT1, and eNOS in insulin resistance, and its epigenetic regulation. However, additional studies are required to confirm that these genes are regulated by DNA methylation.How Does HSP72 Induction Improve ANG-(1-7) Signaling?HS has been shown to inhibit ANG II-induced hypertension and inflammation in the heart and aorta (23,34). This suggests the presence of cross talk between HS and RAS.…”

mentioning

confidence: 99%

“…Over the years, from the discovery of heat shock (HS) response, several studies pointed out the protective role of HS protein (HSP) 72 in various disorders like cardiac ischemia, Huntington disease, hypertension, and diabetes (23)(24)(25). In the study by Bruce et al (26), correlation between decreased HSP72 expression and the degree of insulin resistance has been demonstrated.…”

mentioning

confidence: 99%

“…Chen et al (23,34) for the first time reported the presence of cross talk between HSPs and RAS. Mild heat treatment (41°C) was able to decrease the ANG IIinduced inflammation and hypertension.…”

mentioning

confidence: 99%

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Heat Shock Prevents Insulin Resistance–Induced Vascular Complications by Augmenting Angiotensin-(1-7) Signaling

Karpe

Tikoo

2014

Diabetes

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We have investigated the role of heat shock (HS) in preventing insulin resistance-induced endothelial dysfunction. To the best of our knowledge, we report here for the first time that insulin resistance inhibits vascular HS protein (HSP) 72 expression. HS treatment (41°C for 20 min) restored the HSP72 expression. High-fat diet (HFD)-fed, insulin-resistant rats show attenuated angiotensin (ANG)-(1-7)-induced vasodilator effect, endothelial nitric oxide synthase (eNOS) phosphorylation, AMP-activated protein kinase phosphorylation, and sirtuin 1 (SIRT1) expression. Interestingly, HS prevented this attenuation. We also provide the first evidence that HFD-fed rats show increased vascular DNA methyltransferase 1 (DNMT1) expression and that HS prevented this increase. Our data show that in HFD-fed rats HS prevented loss in the expression of ANG-(1-7) receptor Mas and ACE2, which were responsible for vascular complications. Further, the inhibition of eNOS (L-N G -nitro-L-arginine methyl ester), Mas (A-779), and SIRT1 (nicotinamide) prevented the favorable effects of HS. This suggests that HS augmented ANG-(1-7) signaling via the Mas/eNOS/SIRT1 pathway. Our study, for the first time, suggests that induction of intracellular HSP72 alters DNMT1 expression, and may function as an epigenetic regulator of SIRT1 and eNOS expression. We propose that induction of HSP72 is a novel approach to prevent insulin resistance-induced vascular complications. Insulin resistance is a prominent component of metabolic syndrome, which is characterized by obesity, hypertension, and atherosclerosis. A reciprocal relationship has been established between insulin resistance and endothelial dysfunction, which may lead to cardiovascular disorders (1). Apart from the metabolic actions, insulin performs various important hemodynamic functions such as peripheral vasodilation and increased regional blood flow via stimulation of nitric oxide (NO). Therefore, anything that impairs insulin action is expected to result in endothelial dysfunction and vice versa (2). Insulin has been shown to induce endothelial-dependent vasodilation without affecting endothelium-independent vasodilation. We and others (3,4) have reported that insulin resistance impairs endothelium-dependent vasodilation.Several studies have pointed out active involvement of renin-angiotensin system (RAS) in cardiovascular disorders and insulin resistance (5,6). RAS further splits in two, as follows: angiotensin (ANG) II/ACE1 and ANG-(1-7)/ACE2 axis. ANG-(1-7), acting through receptor Mas (G-protein-coupled), counter-regulates the actions of ANG II. Mas receptor dimerizes with AT 1 receptor and COMPLICATIONS inhibits ANG II signaling, suggesting direct interaction of ANG II and the ANG-(1-7) axis (7). ANG-(1-7) promotes vasodilation and inhibits cell proliferation thrombosis, hence opposing the effects of ANG II (8,9). In endothelial cells, ANG-(1-7) inhibited ANG II-induced c-Src, extracellular signal-related kinase 1/2, and NADPH oxidase by activating SHP-2 phosphatase (10). ANG-(1-7) als...

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“…HS has been shown to inhibit ANG II-induced hypertension and inflammation in the heart and aorta (23,34). This suggests the presence of cross talk between HS and RAS.…”

Section: Discussionmentioning

confidence: 96%

Section: Hs Treatment Improves Ang-(1-7)-induced Vasodilator Responsesmentioning

confidence: 98%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Heat Shock Prevents Insulin Resistance–Induced Vascular Complications by Augmenting Angiotensin-(1-7) Signaling

Karpe

Tikoo

2014

Diabetes

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Soy extract has different effects compared with the isolated isoflavones on the proteome of homocysteine‐stressed endothelial cells

Fuchs

Dirscherl

Schroot³

et al. 2006

Molecular Nutrition Food Res

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Epidemiological studies suggest that soy consumption may provide a protection in the development and progression of atherosclerosis. It is under debate, however, whether the soy isoflavones or other compounds are the "active principle". As apoptosis is a driving force in the process of atherosclerosis, we tested whether a soy extract or a combination of the two predominant isoflavones genistein and daidzein, in concentrations as found in the extract, exert similar or different effects on apoptosis in EA.hy 926 endothelial cells after exposure to the endothelial stressor homocysteine. Plasma membrane disintegration and nuclear fragmentation served as relevant apoptosis markers. To assess whether the extract and the genistein/daidzein mixture differently affect cellular target proteins changed in amount by homocysteine treatment, proteome analysis was performed by two-dimensional gel-electrophoresis and peptide mass fingerprinting of regulated protein spots. Homocysteine induced apoptosis in the cells, and both extract and genistein/daidzein inhibited apoptosis to a comparable extent. Whereas the extract prevented for 10 proteins the changes in expression levels as caused by homocysteine, the genistein/daidzein mixture reversed the homocysteine effects on the proteome for 13 proteins. The cytoskeletal protein matrin 3 and a U5 snRNP-specific 40-kDa protein were the only protein entities where both extract and genistein/daidzein reversed the homocysteine-induced changes in a common way. In conclusion, our studies provide evidence that an isoflavone containing soy extract and isolated isoflavones, despite similar effects on inhibition of homocysteine-induced apoptosis in endothelial cells, affect a quite different spectrum of cellular target proteins.

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Short-term hyperthermia prevents activation of proinflammatory genes in fibroblast-like synoviocytes by blocking the activation of the transcription factor NF-κB

Markovic¹,

Stuhlmeier²

2006

J Mol Med

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Fibroblast-like synoviocytes (FLS) play a key role in the genesis of rheumatoid arthritis (RA). FLS are among the most versatile cells with the potential to activate an array of genes that are able to initiate and propagate inflammation in RA-affected joints. Controlling activation of FLS might hold the key to restraining inflammation in RA-affected joints. In this study, we investigate the effect and mechanisms of short-term hyperthermia on a series of proinflammatory genes in FLS. In vitro experiments demonstrate that exposure of FLS to elevated temperatures for the duration of 30 min prevents activation of a series of genes with proinflammatory properties. Exposure to hyperthermia reduces IL-1beta-induced prostaglandin E2 release, suppresses activation of the adhesion molecules VCAM-1, ICAM-1, the cytokines TNFalpha, IL-1alpha, IL-1beta, IL-8 as well as COX-2 protein synthesis. Real time reverse transcriptase-polymerase chain reaction showed that hyperthermia altered gene expression at the transcriptional level. The amount and the duration of inhibition is gene-specific and lasts for up to 25 h. As to the mechanism of inhibition, electrophoretic mobility shift assay experiments demonstrated that exposure of FLS to hyperthermia prevents IL-1beta-induced NF-kappaB translocation and subsequent DNA binding. Many mechanisms have been shown to be involved in hyperthermia-mediated effects on NF-kappaB-DNA interactions. We demonstrate by Western blot experiments that in FLS, hyperthermia prevents the phosphorylation and subsequent degradation of IkappaBalpha, therefore retaining the NF-kappaB complex in the cytoplasm. Carefully controlled in vivo tests are certainly needed before one can take full advantage of those phenomena; however, the ease by which the temperature in joints can be modulated might offer an opportunity for manipulating inflammatory processes in joints by simple balneological means.

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Heat shock treatment protects against angiotensin II–induced hypertension and inflammation in aorta

Cited by 23 publications

References 45 publications

Heat Shock Prevents Insulin Resistance–Induced Vascular Complications by Augmenting Angiotensin-(1-7) Signaling

Heat Shock Prevents Insulin Resistance–Induced Vascular Complications by Augmenting Angiotensin-(1-7) Signaling

Soy extract has different effects compared with the isolated isoflavones on the proteome of homocysteine‐stressed endothelial cells

Short-term hyperthermia prevents activation of proinflammatory genes in fibroblast-like synoviocytes by blocking the activation of the transcription factor NF-κB

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