Post-infarct treatment with [Pyr1]apelin-13 improves myocardial function by increasing neovascularization and overexpression of angiogenic growth factors in rats

Azizi, Yaser; Faghihi, Mahdieh; Imani, Alireza; Roghani, Mehrdad; Zekri, Ali; Mobasheri, Maryam Beigom; Rastgar, Tayebeh; Moghimian, Maryam

doi:10.1016/j.ejphar.2015.04.034

Cited by 47 publications

(38 citation statements)

References 36 publications

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“…In this study, along with our previous studies [16,21], we have further studied the anti-apoptotic, anti-remodelling, and anti-hypertrophic effects of apelin-13 in improving myocardial function and preserving its structural integrity.…”

Section: Discussionmentioning

confidence: 99%

“…Its beneficial effects, such as reduction of infarct size, improvement of myocardial function, and contractility against myocardial acute ischaemia and ischaemia/reperfusion (I/R) injuries, have been shown in some studies [11][12][13]. Apelin is widely expressed in the endothelium, binds to G protein-coupled receptor (APJ) in endothelial cells, myocardial cells, and smooth muscle cells and activates its following signalling pathways such as PI3K/Akt, activation of nitric oxide (NO) syntheses (eNOS), and NO production [14][15][16]. Apelin/APJ system (expression of apelin and APJ in the serum and myocardial tissue) has been downregulated in severe and uncompensated HF in experimental and clinical studies [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Post-infarct treatment with [Pyr1]apelin-13 exerts anti-remodelling and anti-apoptotic effects in rats’ hearts

Azizi¹,

Imani²,

Fanaei³

et al. 2017

Kardiol Pol

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A b s t r a c tBackground: Ischaemic heart disease is the main cause of mortality in the world. After myocardial infarction (MI) cardiomyocytes apoptosis and ventricular remodelling have occurred. Apelin is a peptide that has been shown to exert cardioprotective effects. Aim:The aim of this study was to investigate the anti-apoptotic and anti-remodelling effects of [Pyr 1 ]apelin-13 in the rat model of post-MI.Methods: Thirty-six male Wistar rats were randomly divided into three groups: (1) ]apelin-13 has anti-hypertrophic, anti-remodelling, and anti-apoptotic effects via overexpression of Apel, Apelr, and Bcl-2 and reduces gene expression of Bax and Casp-3 in the infarcted myocardium, which can in turn lead to repair myocardium.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Post-infarct treatment with [Pyr1]apelin-13 exerts anti-remodelling and anti-apoptotic effects in rats’ hearts

Azizi¹,

Imani²,

Fanaei³

et al. 2017

Kardiol Pol

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“…Importantly, apelin reduced infarct size and increased nitric oxide (NO) level [116]. The same group also reported reduction of fibrosis and increased capillary density in myocardium after [Pyr1]-apelin-13 treatment in rats [118]. In mouse experiment, apelin-13 treatment post MI decreased fibrosis, the area of MI (assessed by the ratio of the infarcted area to left ventricle area) and increased capillary density and cardiac contractility [117].…”

Section: From Animal Models To Human Studiesmentioning

confidence: 88%

Apelinergic system in endothelial cells and its role in angiogenesis in myocardial ischemia

Nováková

Sandhu

Dragomir-Daescu

et al. 2016

Vascular Pharmacology

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“…), tube formation, and regulating vascular integrity (Azizi et al. ). Interestingly, hypoxic mice infused with apelin exhibit increased cardiac output (Alastalo et al.…”

Section: Discussionmentioning

confidence: 99%

“…Apelin plays a critical role in cardiac development, angiogenesis, prosurvival signaling, nitric oxide-dependent vasodilation, and inotropic signaling (Andersen et al 2011;Dalzell et al 2015). In the LV, apelin regulates blood vessel formation after ischemic injury through the upregulation of cell migration (Wang et al 2013), progenitor cell recruitment and differentiation (Li et al 2012), tube formation, and regulating vascular integrity (Azizi et al 2015). Interestingly, hypoxic mice infused with apelin exhibit increased cardiac output (Alastalo et al 2011), making apelin a promising target for cardiopulmonary diseases.…”

Section: Discussionmentioning

confidence: 99%

Isolated heart model demonstrates evidence of contractile and diastolic dysfunction in right ventricles from rats with sugen/hypoxia-induced pulmonary hypertension

et al. 2017

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Although extensively used for the study of left ventricular function, limited experience exists with the isolated heart model in the evaluation of right ventricular (RV) function. In particular, no published experience exists with this tool in sugen/hypoxia‐induced pulmonary hypertension (SuHx‐PH), a frequently used model of severe and progressive PH. We sought to characterize markers of RV contractile and diastolic function in SuHx‐PH and to establish their relationship with markers of maladaptive RV remodeling. Hearts were excised from anesthetized Sprague Dawley rats with or without SuHx‐PH and perfused via the aorta using a Langendorff preparation. We explored the Frank–Starling relationship of RV function (RV developed pressure, dP/dt max, and dP/dt min; all normalized to RV mass) by increasing RV end‐diastolic pressure (RVEDP) from 0 to 40 mmHg. Functional studies were complemented by quantification of RV pro‐apoptotic signaling (bcl2/bax), procontractile signaling (apelin), and stress response signaling (p38MAPK activation). Pearson's correlation analysis was performed for functional and biochemical parameters. SuHx‐RVs exhibited severe RV dysfunction with marked hypertrophy and decreased echocardiographic cardiac output. For any given RVEDP, SuHx‐RVs demonstrated less developed pressure and lower dP/dt max, as well as less pronounced dP/dt min, suggestive of decreased contractile and diastolic function. SuHx‐RVs exhibited decreased bcl2/bax ratios, apelin expression, and p38MAPK activation. Bcl2/bax and apelin RNA abundance correlated positively with RV developed pressure and dP/dt max and negatively with dP/dt min. p38MAPK activation correlated positively with RV developed pressure. We conclude that SuHx‐RVs exhibit severe contractile and diastolic dysfunction. Increased pro‐apoptotic signaling and attenuated procontractile and stress response signaling may contribute to these functional alterations.

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Post-infarct treatment with [Pyr1]apelin-13 improves myocardial function by increasing neovascularization and overexpression of angiogenic growth factors in rats

Cited by 47 publications

References 36 publications

Post-infarct treatment with [Pyr1]apelin-13 exerts anti-remodelling and anti-apoptotic effects in rats’ hearts

Post-infarct treatment with [Pyr1]apelin-13 exerts anti-remodelling and anti-apoptotic effects in rats’ hearts

Apelinergic system in endothelial cells and its role in angiogenesis in myocardial ischemia

Isolated heart model demonstrates evidence of contractile and diastolic dysfunction in right ventricles from rats with sugen/hypoxia-induced pulmonary hypertension

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