Hydrogen peroxide induces tumor necrosis factor α–mediated cardiac injury by a P38 mitogen-activated protein kinase–dependent mechanism

Meldrum, Daniel R.; Dinarello, Charles A.; Cleveland, Joseph C.; Cain, Brian S.; Shames, Brian D.; Meng, Xianzhong; Harken, Alden H.

doi:10.1016/s0039-6060(98)70133-3

Cited by 102 publications

(69 citation statements)

References 20 publications

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“…32 Apparently, inflammatory cytokines can induce oxidative stress-for example, TNF-a can directly induce the production of mitochondrial reactive oxygen species in the cardiomyocytes, causing damage to the mitochondrial DNA, 33 -whereas oxidative stress can increase the levels of inflammatory cytokines, leading to the development of a vicious cycle in the failing hearts. 34,35 In this study, the anti-oxidative effect of Ang (1-7) may be attributed to its anti-inflammation effect. However, Ang (1-7) may directly inhibit the oxidative stress.…”

Section: Angiotensin (1à7) Prevent Heart Dysfunction and Left Ventricmentioning

confidence: 72%

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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The renin-angiotensin system (RAS) plays a critical role in chronic renal failure associated with heart failure. In the past few years, angiotensin (Ang) (1-7) have been reported to counteract the effects of angiotensin II (Ang II) and were even considered as a new therapeutical target in RAS. The purposes of this study were to examine whether the Ang (1-7) improves the heart function and remodeling of the left ventricle (LV) in mice with 5/6 nephrectomy (NC). We used a 5/6 nephrectomy to induce significant renal dysfunction in wildtype mice (WT). Twelve weeks after NC, WT showed high blood pressure, significant leftventricular dilation and dysfunction, which were accompanied by cardiomyocyte hypertrophy, diffuse interstitial fibrosis and oxidative damage of cardiomyocytes. Exogenous Ang (1-7) injection improved the heart function and remodeling of LV in mice with 5/6 NC accompanied by a reduction in cardiac interstitial fibrosis, inflammatory cytokine expression and oxidative damage levels of cardiomyocytes, decrease in the profibrotic signaling molecule transforming growth factor (TGF)-b and increase in the collagen degradation signaling molecule matrix metalloproteinase (MMP)-2, -9. However, these beneficial effects did not occur in hydralazine-treated mice. These findings suggest that (1) Exogenous Ang (1-7) injection improve the heart function and remodeling of LV in mice with 5/6 NC. (2) These beneficial effects are independent of its anti-blood pressure effect.

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Section: Angiotensin (1à7) Prevent Heart Dysfunction and Left Ventricmentioning

confidence: 72%

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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“…[10][11][12]16,[18][19][20][21][22][23][24] For example, in cultured neonatal rat ventricular myocytes, MAPKs are activated by growth factors such as angiotensin II, endothelin-1 and -adrenergic agonists, and by cellular stress such as ultraviolet irradiation, reactive oxygen species, mechanical stretch, electrical pacing, and hyperosmotic shock. [25][26][27][28][29][30][31][32] Regarding ischemic heart disease, we previously reported that myocardial ERKs, JNKs and p38MAPK are activated in the infarcted myocardium of rat hearts, followed by activation of AP-1 and increased mRNA expression of transforming growth factor -1, collagen types I and III, atrial natriuretic peptide, -myosin heavy chain, and -skeletal actin. 8 In addition, we also reported increased mRNA levels for -skeletal actin, atrial natriuretic peptide, collagen types I and III in the noninfarcted myocardium 2 days after the infarction.…”

Section: Discussionmentioning

confidence: 99%

Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in Rats.

Yoshida¹,

Yoshiyama²,

Omura³

et al. 2001

Jpn Circ J

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fter myocardial infarction (MI), contractile impairment in the ischemic myocardium (IM) occurs suddenly and the non-ischemic myocardium adapts to the increased workload. Thereafter, the myocardial properties and morphology begin to change as the ventricular remodeling during the clinical course. The ventricular remodeling is accompanied by progressive chamber dilatation and subsequently an increased incidence of sudden death and congestive heart failure. [1][2][3][4][5] In the IM, the structural rearrangement is characterized by myocardial cell damage, inflammatory change and expression of extracellular matrix components. Furthermore, ventricular dilatation and myocardial hypertrophy can occur in the non-ischemic regions. 6 The process of ventricular remodeling after an acute myocardial infarction (AMI) involves topographical alternations in the ischemic and non-ischemic regions, 1,2 so an understanding of the myocardial response to AMI is important for appropriate therapeutic management.We previously reported that mitogen-activated protein kinases (MAPKs) are rapidly activated in the IM, followed by activation of transcriptional factors of activator protein 1 (AP-1) and mRNA expression of transforming growth factor -1, collagen types I and III, -myosin heavy chain, -skeletal actin and atrial natriuretic peptide. 7,8 MAPKs are a ubiquitous group of protein serine/threonine kinases and are important mediators of the signal transduction pathways responsible for cell growth, proliferation and apoptosis. [9][10][11][12] Therefore, this signal transduction system may be a key regulatory mechanism allowing cells to respond and eventually adapt to changes in myocardial ischemia. Although enhanced expression of the mRNAs was also observed in the non-ischemic region of the acutely infarcted heart, 7,8,13 the corresponding activities of MAPKs in that region are still unknown. The present study investigated whether the signal-transduction pathway of the non-ischemic myocardium shifted to ventricular remodeling after AMI by examining the myocardial activities of extracellular signal-regulated kinases (ERKs), c-Jun NH2 terminal kinases (JNKs) and p38MAPK, plus the AP-1 DNA binding activities in both the ischemic and non-ischemic regions of an infarcted rat heart. Furthermore, to clarify the possible cause of MAPKs activation, we measured the geometrical changes of the infarcted heart using echocardiography and then estimated the stretch and workload of the infarcted heart. Methods Production of the AMIMale Wistar rats weighing 290-310g (Clea Japan, Osaka, Japan) were used in the experiments. Myocardial infarction was produced as described previously. 7,8,14 Briefly, the rats were anesthetized by intraperitoneal injection of pentobarbital sodium (35 mg/kg). After intratracheal intubation, a left thoracotomy was performed under volume-controlled Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in RatsKen Yoshida, MD; Minoru Yoshiyama, MD; Takashi Omura, MD; Yasuh...

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“…Thus, we conclude that a pro-oxidant environment created by treatment with diazoxide is required for diazoxidemediated cardioprotection. Specific signaling targets for redoxmediated changes involved in this protective effect have not been elucidated but may include protein kinase C, 22 p38 mitogen-activated protein kinase, 21 and K ϩ ATP channels. 44 …”

Section: Attenuation Of Ischemic Acidification By Diazoxidementioning

confidence: 99%

“…Fluctuations in oxidant/antioxidant balance are known to influence the activation of transcription factors nuclear factor-B, activator protein-1, and hypoxia-inducible factor-1 19,20 ; protein kinases and phosphatases [21][22][23] ; Ca 2ϩ , K ϩ , and Na ϩ channels 24 -27 ; and Na ϩ -Ca 2ϩ exchanger, 28 as well as GAPDH and pyruvate dehydrogenase. 29 ROS generated during preconditioning cycles of ischemia/reperfusion have been implicated in the triggering of the observed cardioprotective effects.…”

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confidence: 99%

Diazoxide-Induced Cardioprotection Requires Signaling Through a Redox-Sensitive Mechanism

Forbes

Steenbergen

Murphy

2001

Circulation Research

353

236

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Abstract-Diazoxide, a selective opener of the mitochondrial ATP-sensitive potassium channel, has been shown to elicit tolerance to ischemia in cardiac myocytes and in perfused heart. However, the mechanism of this cardioprotection is poorly understood. Because reactive oxygen species (ROS) are recognized as important intracellular signaling molecules and have been implicated in ischemic preconditioning, we examined diazoxide-induced ROS production in adult cardiomyocytes. Cells treated with 50 mol/L diazoxide showed a 173% increase in ROS production relative to baseline. 5-Hydroxydecanoate was found to attenuate the diazoxide-induced increase in ROS generation. The diazoxide-induced increase in ROS also was abrogated by the addition of either the antioxidant N-acetylcysteine (NAC) or N-mercaptopropionylglycine. We also examined the ability of NAC to block the protective effects of diazoxide in the perfused rat heart. After 20 minutes of global ischemia and 20 minutes of reflow, hearts perfused with 100 mol/L diazoxide before ischemia showed significantly improved postischemic contractile function relative to untreated hearts (84% versus 29% of initial left ventricular developed pressure, respectively). Hearts treated with diazoxide in the presence of 4 mmol/L NAC recovered 53% of initial left ventricular developed pressure, whereas hearts treated with NAC alone recovered 46% of preischemic function. Using 31 P NMR spectroscopy, we found that, similar to preconditioning, diazoxide significantly attenuated ischemia-induced intracellular acidification and enhanced postischemic recovery of phosphocreatine levels, both of which were blocked by cotreatment with NAC. These data suggest that the cardioprotective actions of diazoxide are mediated by generation of a pro-oxidant environment.

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Hydrogen peroxide induces tumor necrosis factor α–mediated cardiac injury by a P38 mitogen-activated protein kinase–dependent mechanism

Cited by 102 publications

References 20 publications

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in Rats.

Diazoxide-Induced Cardioprotection Requires Signaling Through a Redox-Sensitive Mechanism

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