Angiotensin II Type 2 Receptor (AT2R) is Associated with Increased Tolerance of the Hyperthyroid Heart to Ischemia-Reperfusion

Tavares, Felix Meira; Silva, Ivson Bezerra da; Gomes, Dayane Aparecida; Barreto‐Chaves, Maria Luíza Morais

doi:10.1007/s10557-013-6473-x

Cited by 21 publications

(22 citation statements)

References 44 publications

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“…This effect was associated with increased intracellular Ca 2+ level, which subsequently increased contractility and enhanced energy demands. It is well established that AMPK acts as a fuel gauge for the cell, thus it is also an important regulator of myocardial energy metabolism by promoting glucose uptake and glycolysis as well as fatty acid oxidation [50]. Our research confirms that prolonged T 3 treatment has the ability to alter the phosphorylation status of AMP kinase in myocardium, tissue with high-oxidative capacity.…”

Section: Discussionsupporting

confidence: 82%

Hyperthyroidism Evokes Myocardial Ceramide Accumulation

Mikłosz

Łukaszuk

Chabowski

et al. 2015

Cell Physiol Biochem

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Background: Thyroid hormones (THs) are key regulators of cardiac physiology as well as modulators of different cellular signals including the sphingomyelin/ceramide pathway. The objective of this study was to examine the effect of hyperthyroidism on the metabolism of sphingolipids in the muscle heart. Methods: Male Wistar rats were treated for 10 days with triiodothyronine (T₃) at a dose of 50µg/100g of body weight. Animals were then anaesthetized and samples of the left ventricle were excised. Results: We have demonstrated that prolonged, in vivo, T₃ treatment increased the content of sphinganine (SFA), sphingosine (SFO), ceramide (CER) and sphingomyelin (SM), but decreased the level of sphingosine-1-phosphate (S1P) in cardiac muscle. Accordingly, the changes in sphingolipids content were accompanied by a lesser activity of neutral sphingomyelinase and without significant changes in ceramidases activity. Hyperthyroidism also induced activation of AMP-activated protein kinase (AMPK) with subsequently increased expression of mitochondrial proteins: cytochrome c oxidase IV (COX IV), β-hydroxyacyl-CoA dehydrogenase (β-HAD), carnityne palmitoyltransferase I (CPT I) and nuclear peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α). Conclusions: We conclude that prolonged T₃ treatment increases sphingolipids metabolism which is reflected by higher concentration of SFA and CER in heart muscle. Furthermore, hyperthyroidism-induced increase in heart sphingomyelin (SM) concentration might be one of the mechanisms underlying maintenance of CER at relatively low level by its conversion to SM together with decreased S1P content.

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Section: Discussionsupporting

confidence: 82%

Hyperthyroidism Evokes Myocardial Ceramide Accumulation

Mikłosz

Łukaszuk

Chabowski

et al. 2015

Cell Physiol Biochem

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“…The ascending aorta was cannulated to attach the heart to a non-recirculating water-jacketed, constant flow Langendorff apparatus (Radnotti; Harvard Apparatus USA). Hearts were perfused with a Kreb-Henseleit buffer (pH 7.4) aerated with a mixture of 95% O 2 -5% CO2 [14] . A saline filled latex balloon connected to a pressure transducer (Ad Instruments, MLT0380, Australia) was inserted into the left ventricle through an incision in the left atrial appendage.…”

Section: Ex-vivo Cardiac Contractility Assessmentmentioning

confidence: 99%

Resveratrol Improves Cardiac Functions of the Diabetic Cardiomyopathy Rats Via Modulation of AMP-Activated Protein Kinase and the Phosphorylated Glycogen Synthase Kinase-3(3

Shamseldeen¹,

Rashed²,

Elsayed³

et al. 2019

The Medical Journal of Cairo University

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Background: Resveratrol (RSV) has a wide range of diabetic cardioprotective effects. It is currently recognized as a dietary supplement. Aim of Study:To investigate the impact of RSV on the molecular expression pattern of AMP-activated protein kinase (AMPK) and the glycogen synthase kinase-3 (3 serine 9 (GSK-3 (3 S9) in diabetic cardiomyopathy. Methods:We investigated this point using three groups of Wistar albino rats; control group, diabetic cardiomyopathy rats (DCM) and diabetics treated with RSV (DM-RSV) for 20 weeks. Echocardiography was performed at base line, and every 4 weeks. At the end of the study, Ex-vivo assessment of myocardial contractility was performed. The molecular changes in the cardiac tissues were evaluated in all groups for assessment of the silent information regulator (SIRT1), GSK-3 (3 S9 and the AMPK levels. Histological assessment was done for all cardiac tissues. Apoptosis was assessed by measuring the modulation in the Bax/Bcl2 ratio and poly (ADP-ribose) polymerase-1 (PARP1) levels, trying to explore the RSV underlying mechanism of action.Results: Marked deterioration in the cardiac functions was detected in the diabetic non treated group. The decreased levels of SIRT1, AMPK and GSK-3 (3 S9 that was associated with increased apoptotic markers, may be the cause of deteriorated cardiac functions. Assessment of the myocardial functions showed improvement in the diabetic RSV treated group. RSV aimed to normalize the hyperglycemic state and the disturbed molecular pattern associated with diabetes.Conclusion: Prolonged RSV administration protects the diabetic hearts. This could be explained by the interplay between SIRT1, AMPK and the GSK-3(3 S9 levels.

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“…AT2R-dependent cell signaling and effects are less studied than those of the AT1R [138,139], but has vasodilation, anti-proliferative and anti-inflammatory effects [140,141]. Moreover, recent studies showed that AT2R regulates BP, cardiac hypertrophy and fibrosis, and cell death after MI [142,143]. Such effects could be mediated by increased production of NO and vasodilation [144][145][146].…”

Section: Angiotensin Type 2 Receptor (At2r)mentioning

confidence: 99%