Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Bhuiyan, Md. Shenuarin; Fukunaga, Kohji

doi:10.1254/jphs.09r01cr

Cited by 61 publications

(30 citation statements)

References 131 publications

(180 reference statements)

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“…Our results showed that PCA significantly decreased hypoxia/ reoxygenation-induced cardiomyocyte apoptotic rate and the expression of cleaved caspase-3. Akt protein kinase is an important mediator of cardiomyocyte growth and survival (34,35). Previous studies indicated that activation of Akt could suppress apoptosis and promote survival of cardiomyocytes in ischemic heart disease (36).…”

Section: Discussionmentioning

confidence: 99%

The Cardioprotective Effect of Protocatechuic Acid on Myocardial Ischemia/Reperfusion Injury

et al. 2014

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Abstract. Protocatechuic acid (PCA), a phenolic compound and one of the main metabolites of complex polyphenols, has been found to possess various biological activities, and it may have a potential in the treatment of ischemic heart diseases. This study explored the cardioprotective effect of PCA on myocardial ischemia/reperfusion (MI/R) injury and the underlying mechanisms. In an in vivo rat model of MI/R injury, myocardial infarct size, serum TNF-a level, and platelet aggregation were measured. In a primary neonatal rat cardiomyocyte model of hypoxia/ reoxygenation (H/R) injury, the apoptotic rate, expressions of cleaved caspase-3, and phosphorylated Akt were observed. We found that PCA significantly reduced myocardial infarct size, serum TNF-a level, and platelet aggregation. In vitro experiments revealed that PCA significantly inhibited the apoptotic rate and the expression of cleaved caspase-3, and it upregulated the expression of phosphorylated Akt in cardiomyocytes subjected to H/R injury. Our results suggest that PCA can provide a significant protection against MI/R injury, which may be at least partially attributed to its inhibitions against injury induced by MI/R including the inflammatory response, platelet aggregation, and cardiomyocytes apoptosis.

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Section: Discussionmentioning

confidence: 99%

The Cardioprotective Effect of Protocatechuic Acid on Myocardial Ischemia/Reperfusion Injury

et al. 2014

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“…The pharmacological beta-AR agonist and blockers are in clinical practice for maintaining the sympathetic drive in cardiovascular diseases [4;29]. The empirical evidences suggest their role in diabetic cardiomyopathy [3]. During heart failure there is remarkable down regulation of beta-AR [4;29].…”

Section: Discussionmentioning

confidence: 99%

Attenuation of beta2-adrenergic receptors and homocysteine metabolic enzymes cause diabetic cardiomyopathy

Mishra

Givvimani

Metreveli

et al. 2010

Biochemical and Biophysical Research Communications

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Although adrenergic receptors (AR) and hyperhomocysteinemia (HHcy) are implicated in heart failure, their role in diabetic cardiomyopathy is not completely understood. We tested the hypothesis that glucose mediated depletion of beta2-AR and HHcy impair contractile function of cardiomyocytes leading to diabetic cardiomyopathy. To prove the hypothesis, cardiac function was assessed in twelve week male diabetic Ins2+/− Akita and C57BL/6J mice by echocardiography, pressure-volume loop and contractile function of cardiomyocytes. The results revealed cardiac dysfunction in Akita. To investigate the mechanism, the levels of beta2-AR, GLUT4, sercoplasmic reticulum calcium ATP-ase –isoform 2 (SERCA-2) and homocysteine (Hcy) metabolic enzymes -cystathionine beta synthase (CBS), cystathionine gamma lyase (CTH) and methyl tetrahydrofolate reductase (MTHFR) were determined in the heart. It revealed down regulation of beta2-AR, GLUT4, SERCA-2, CBS, CTH and MTHFR in Akita. Attenuation of beta2-AR in hyperglycemic condition was also confirmed in cardiomyocytes at in vitro level. Interestingly, the ex vivo treatment of cardiomyocytes with beta2-AR antagonist deteriorated whereas beta-AR agonist ameliorated contractile function. It points to the involvement of beta2-AR in diabetic cardiomyopathy. We conclude that degradation of beta2-AR and impairment of Hcy metabolism is implicated in diabetic cardiomyopathy.

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“…There are various studies indicating a potential relationship between cardiac hypertrophy, angiogenesis, and cardiac dysfunction, but the mechanisms by which cardiac hypertrophy develops into congestive heart failure are still unclear (7,8,28,29). It has been postulated that for the purpose of maintaining cardiac function, cardiac hypertrophy occurred (1), which led to myocardial hypoxia because of the mismatch between cardiac angiogenesis and the increased size of cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

A Potential Role of Alpha-7 Nicotinic Acetylcholine Receptor in Cardiac Angiogenesis in a Pressure-Overload Rat Model

Yang

et al. 2010

J Pharmacol Sci

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Abstract. This work investigated the expression of alpha-7 nicotinic acetylcholine receptor (α7nAChR) in the left ventricle and its putative role in cardiac angiogenesis in a pressure overload rat model induced by abdominal aorta coarctation. Blood pressure and protein levels of α7nAChR were measured at 4, 8, 12, and 16 weeks after surgery. mRNA levels of α7nAChR, cardiac vagus nerve function, cardiac hypertrophy, and microvessel density of the left ventricle were determined at the final 16-week period. The role of α7nAChR in angiogenesis was evaluated. It was found that systolic blood pressure above the coarctation site was greater at 16 weeks after coarctation and expression of α7nAChR was significantly increased at both mRNA and protein levels in the left ventricle compared with the control. Positive staining for receptors was mainly focused around vessels and among the degenerated cardiomyocytes. Cardiac vagus nerve function was significantly attenuated; microvessel density was markedly increased and was associated with cardiac hypertrophy. Activation of α7nAChR induced tube formation of cultured human umbilical vein endothelial cells (HUVECs). We conclude that expression of α7nAChR was increased at 16 weeks after coarctation, and this might be a compensatory response to decreased vagus nerve function and cardiac hypertrophy and may also play a role in cardiac angiogenesis.

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Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Cited by 61 publications

References 131 publications

The Cardioprotective Effect of Protocatechuic Acid on Myocardial Ischemia/Reperfusion Injury

The Cardioprotective Effect of Protocatechuic Acid on Myocardial Ischemia/Reperfusion Injury

Attenuation of beta2-adrenergic receptors and homocysteine metabolic enzymes cause diabetic cardiomyopathy

A Potential Role of Alpha-7 Nicotinic Acetylcholine Receptor in Cardiac Angiogenesis in a Pressure-Overload Rat Model

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