Modulation of cardiac stem cell characteristics by metoprolol in hypertensive heart disease

Saheera, Sherin; Potnuri, Ajay Godwin; Nair, R. V.

doi:10.1038/s41440-018-0015-7

Cited by 12 publications

(20 citation statements)

References 35 publications

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“…Metoprolol is a selective β1-adrenoceptor inhibitor, that has been widely used to improve heart function [36,37]. Many studies have shown that long-term treatment with Met could downregulate collagen I and III mRNA levels, and modulate stem cell characteristics to prevent progressive pathological remodeling, in addition, Met could improve the Ca 2+ handling and contractility of right ventricular (RV) myocytes isolated from monocrotaline (MCT)-treated rats [18,[38][39][40]. In embryonic development, β-adrenoceptor stimulation leads to decreased AKT phosphorylation [41].…”

Section: Discussionmentioning

confidence: 99%

Metoprolol alleviates arginine vasopressin-induced cardiomyocyte hypertrophy by upregulating the AKT1–SERCA2 cascade in H9C2 cells

et al. 2020

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Background: Arginine vasopressin (AVP) is elevated in patients with heart failure, and the increase in the AVP concentration in plasma is positively correlated with disease severity and mortality. Metoprolol (Met) is a beta blocker that is widely used in the clinic to treat pathological cardiac hypertrophy and to improve heart function. However, the specific mechanism by which Met alleviates AVP-induced pathological cardiac hypertrophy is still unknown. Our current study aimed to evaluate the inhibitory effects of Met on AVP-induced cardiomyocyte hypertrophy and the underlying mechanisms. Methods: AVP alone or AVP plus Met was added to the wild type or AKT1-overexpressing rat cardiac H9C2 cell line. The cell surface areas and ANP/BNP/β-MHC expressions were used to evaluate the levels of hypertrophy. Western bolting was used to analyze AKT1/P-AKT1, AKT2/P-AKT2, total AKT, SERCA2, and Phospholamban (PLN) expression. Fluo3-AM was used to measure the intracellular Ca 2+ stores. Results: In the current study, we found that AKT1 but not AKT2 mediated the pathogenesis of AVP-induced cardiomyocyte hypertrophy. Sustained stimulation (48 h) with AVP led to hypertrophy in the H9C2 rat cardiomyocytes, resulting in the downregulation of AKT1 (0.48 fold compared to control) and SERCA2 (0.62 fold), the upregulation of PLN (1.32 fold), and the increase in the cytoplasmic calcium concentration (1.52 fold). In addition, AKT1 overexpression increased the expression of SERCA2 (1.34 fold) and decreased the expression of PLN (0.48 fold) in the H9C2 cells. Moreover, we found that Met could attenuate the AVP-induced changes in AKT1, SERCA2 and PLN expression and decreased the cytoplasmic calcium concentration in the H9C2 cells. Conclusions: Our results demonstrated that the AKT1-SERCA2 cascade served as an important regulatory pathway in AVP-induced pathological cardiac hypertrophy.

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Section: Discussionmentioning

confidence: 99%

Metoprolol alleviates arginine vasopressin-induced cardiomyocyte hypertrophy by upregulating the AKT1–SERCA2 cascade in H9C2 cells

et al. 2020

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“…The transplantation of CPC into an infarcted myocardium can improve myocardial contractility and ventricular remodeling, inhibit inflammation, and increase CM survival, myogenesis and angiogenesis/neovascularization. Saheera S et al found that oxidative stress and senescence of CSCs were alleviated after treatment with metoprolol, which increased the migration and proliferation of CSCs and was beneficial in delaying progressive cardiac remodeling [148]. Insulin-like growth factor-1 is a synthetic growth hormone that regulates cell proliferation, differentiation, senescence and death; Sun Y et al found that IGF-1 promotes the proliferation and migration of CSCs by activating the PI3K/AKT/DNMT signaling pathway [149].…”

Section: Cscsmentioning

confidence: 99%

Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease

Yan¹,

Xu²,

Huang³

2021

Aging and disease

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Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.

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“…According to the preliminary criteria for the study, 410 patients were tested for exercise. GMJ.2020;9:e1323 www.gmj.ir 3 The exercise test results were interpreted in these specimens. After interpreting the results, 50 patients were excluded from the study due to positive test results.…”

Section: Sample Sizementioning

confidence: 99%

“…The interaction between genetic factors and hemodynamic factors causes heart disease caused by HTN in patients with arterial hypertension [ 1 , 2 ]. The result of structural and functional adaptation leads to increased left ventricular mass (LVM), diastolic dysfunction, congestive heart failure (CHF), arrhythmia, and myocardial perfusion disorders due to dysfunction of the subendothelial vessels [ 3 , 4 ]. However, HTN is one of the major causes of heart failure and the mortality caused by this problem, especially when it first occurs and persists over a number of years without clinical sign and treatment, in which case life expectancy is reduced by an average of 10 – 20 years [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…It has also been well documented that the structural and functional abnormalities of the heart in primary blood pressure increase the risk of mortality and morbidity [ 12 ]. However, there is no clear relationship between the known blood pressure in the clinic and the level of structural and functional compliance of the left ventricle [ 1 , 3 , 6 , 10 , 12 ]. Reduced systolic function of the left ventricle is due to initial hypertension in the final stages of the disease.…”

Section: Introductionmentioning

confidence: 99%

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The Relationship between Left Ventricular Function Indices in Tissue Doppler Imaging and Exaggerated Blood Pressure Response During the Exercise Stress Test

Hemati

Gholoobi

Eshraghi

et al. 2020

GMJ

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Background: Studies have indicated that exaggerated hypertension during activity and stress can be a good predictor of the incidence of hypertension. This study tries to evaluate left ventricular (LV) function by tissue Doppler to assess early changes in ventricular compliance before the onset of Hypertension (HTN) in patients with exaggerated blood pressure response during the exercise test. Materials and Methods: In this case-control study, 40 patients without a history of hypertension with systolic blood pressure less than 140/90 which referred for exercise test, were included. The exercise test was performed for all patients. Patients who had exaggerated blood pressure during the stress test were considered as cases and the controls with normal blood pressure responses. Then standard echocardiography and Tissue Doppler imaging performed and indices of LV systolic and diastolic were recorded. Results: The LV mass in cases and controls were 174.9±50.78 and 152.9±33.59, respectively (P=0.114), and LV mass index in cases and controls were 127.4±13.5 and 79.8±15.75, respectively (P=0.023). Moreover, the LV Myocardial Performance Index were 0.68±0.11 and 0.48±0.06 in cases and controls, respectively (P<0.001). The heart rate, E/A, EE, E Velocity and S velocity were measuremented. Except E/A (P=0.009), there was no significant difference between the other variables measured between the cases and controls (P>0.05). Conclusion: The results of this study showed that using 2D conventional echocardiography as a noninvasive method if performed in prestigious centers can evaluate systolic and diastolic function Tissue Doppler parameters very well in the early stages of heart disease caused by HTN. [GMJ.2020;9:e1323]

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Modulation of cardiac stem cell characteristics by metoprolol in hypertensive heart disease

Cited by 12 publications

References 35 publications

Metoprolol alleviates arginine vasopressin-induced cardiomyocyte hypertrophy by upregulating the AKT1–SERCA2 cascade in H9C2 cells

Metoprolol alleviates arginine vasopressin-induced cardiomyocyte hypertrophy by upregulating the AKT1–SERCA2 cascade in H9C2 cells

Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease

The Relationship between Left Ventricular Function Indices in Tissue Doppler Imaging and Exaggerated Blood Pressure Response During the Exercise Stress Test

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