scholarly journals Effects of chronic inhibition of Testosterone metabolism on cardiac remodeling after ischemia/reperfusion-induced myocardial damage in gonadectomized rats

Biology Open ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. bio041905
Author(s):  
Octavio Maldonado ◽  
Angel Ramos ◽  
Mario Guapillo ◽  
Jose Rivera ◽  
Icela Palma ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Testosterone Metabolism

Overexpression of miR-431 attenuates hypoxia/reoxygenation-induced myocardial damage via autophagy-related 3

2020 ◽  
Author(s):  
Kang Zhou ◽  
Yan Xu ◽  
Qiong Wang ◽  
Lini Dong
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Protective Role ◽  
Human Cardiomyocytes ◽  
Hypoxia Reoxygenation

Abstract Myocardial injury is still a serious condition damaging the public health. Clinically, myocardial injury often leads to cardiac dysfunction and, in severe cases, death. Reperfusion of the ischemic myocardial tissues can minimize acute myocardial infarction (AMI)-induced damage. MicroRNAs are commonly recognized in diverse diseases and are often involved in the development of myocardial ischemia/reperfusion injury. However, the role of miR-431 remains unclear in myocardial injury. In this study, we investigated the underlying mechanisms of miR-431 in the cell apoptosis and autophagy of human cardiomyocytes in hypoxia/reoxygenation (H/R). H/R treatment reduced cell viability, promoted cell apoptotic rate, and down-regulated the expression of miR-431 in human cardiomyocytes. The down-regulation of miR-431 by its inhibitor reduced cell viability and induced cell apoptosis in the human cardiomyocytes. Moreover, miR-431 down-regulated the expression of autophagy-related 3 (ATG3) via targeting the 3ʹ-untranslated region of ATG3. Up-regulated expression of ATG3 by pcDNA3.1-ATG3 reversed the protective role of the overexpression of miR-431 on cell viability and cell apoptosis in H/R-treated human cardiomyocytes. More importantly, H/R treatments promoted autophagy in the human cardiomyocytes, and this effect was greatly alleviated via miR-431-mimic transfection. Our results suggested that miR-431 overexpression attenuated the H/R-induced myocardial damage at least partly through regulating the expression of ATG3.

Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia–reperfusion in vivo

2012 ◽  
Vol 107 (4) ◽  
Author(s):  
Martinus I. F. J. Oerlemans ◽  
Jia Liu ◽  
Fatih Arslan ◽  
Krista Ouden ◽  
Ben J. Middelaar ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Remodeling ◽  
Ischemia Reperfusion ◽  
Myocardial Ischemia Reperfusion

Abstract 141: Inhibition of Coagulation Factor Xa Attenuates Myocardial Ischemia Reperfusion Injury in Mice

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Jens Posma ◽  
Jelle Posthuma ◽  
Rene Van Oerle ◽  
Stefan Heitmeier ◽  
Hugo Ten Cate ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coagulation Factor ◽  
Myocardial Damage ◽  
Reperfusion Therapy ◽  
Coagulation Cascade ◽  
Early Model ◽  
Area At Risk ◽  
Protease Activated Receptors ◽  
Tetrazolium Chloride

Background: Ischemic/reperfusion (I/R) injury substantially effects the outcome of myocardial infarction (MI). Current reperfusion therapy does not sufficiently prevent injury caused by microvascular thrombo-inflammation. Coagulation proteases mediate inflammation via protease activated receptors. FXa induced thrombin generation is the key step in the coagulation cascade. We hypothesize that inhibition of FXa by rivaroxaban attenuates I/R injury after MI. Methods: Male WT c57BL/6 mice (age 8-9 weeks, n=8 per group) underwent surgical ligation of the left anterior descending coronary artery 7 days prior to experimentation. Next, the ligature was tightened for 1h to induce ischemia and loosened either at 4h (early), or at 4 weeks (late), to allow reperfusion. The intervention consisted of 2 rivaroxaban (1.6 mg/kg) i.v.-injections or placebo (0.9%NaCl) after 15min of ischemia and 5min of reperfusion. In the early model. the area at risk (AAR) was visualized through Evans blue and differentiated from the area of infarction (AOI) through triphenyl tetrazolium chloride staining. Plasma cardiovascular markers were quantified using Luminex Multiplex. In the late model, LVEF was measured 10min pre-ischemia and 4 weeks’ post-reperfusion utilizing echocardiography. Results: The rivaroxaban treatment group showed signs of diminished myocardial damage as indicated by reduced median AOI/AAR (41%[IQR34-48] vs. control 62%[IQR52-67] p<0.001). This was supported by a better preserved LVEF after 4 weeks of reperfusion (25%[IQR19-31] vs. control (16%[IQR12-21]). Although not significantly different, plasma E-Selectin, PECAM-1, PAI-1, proMMP9, and thrombomodulin showed a trend to increased levels upon treatment with rivaroxaban. Conclusion: FXa inhibition by rivaroxaban significantly reduces myocardial I/R injury in mice and may provide long term preservation of LVEF. Raised cardiovascular markers suggest increased tissue remodeling and phenotypical alteration of endothelial cells after rivaroxaban treatment. These results suggest that coagulation proteases (i.e. FXa) play a relevant role in I/R injury during MI, most likely through activation of protease activated receptors.

scholarly journals Targeting chronic cardiac remodeling with cardiac progenitor cells in a murine model of ischemia/reperfusion injury

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0173657 ◽  
Author(s):  
Janine C. Deddens ◽  
Dries A. Feyen ◽  
Peter-Paul Zwetsloot ◽  
Maike A. Brans ◽  
Sailay Siddiqi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Progenitor Cells ◽  
Murine Model ◽  
Cardiac Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Progenitor Cells

Role of intracellular antioxidant enzymes after in vivo myocardial ischemia and reperfusion

2003 ◽  
Vol 284 (1) ◽  
pp. H277-H282 ◽  
Author(s):  
Steven P. Jones ◽  
Michaela R. Hoffmeyer ◽  
Brent R. Sharp ◽  
Ye-Shih Ho ◽  
David J. Lefer
Keyword(s):  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Ischemia Reperfusion ◽  
Myocardial Necrosis ◽  
Myocardial Damage ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

Reactive oxygen species induce myocardial damage after ischemia and reperfusion in experimental animal models. Numerous studies have investigated the deleterious effects of ischemia-reperfusion (I/R)-induced oxidant production using various pharmacological interventions. More recently, in vitro studies have incorporated gene-targeted mice to decipher the role of antioxidant enzymes in myocardial reperfusion injury. We examined the role of cellular antioxidant enzymes in the pathogenesis of myocardial I/R (MI/R) injury in vivo in gene-targeted mice. Neither deficiency nor overexpression of Cu-Zn superoxide dismutase (SOD) altered the extent of myocardial necrosis. Overexpression of glutathione peroxidase did not affect the degree of myocardial injury. Conversely, overexpression of manganese (Mn)SOD significantly attenuated myocardial necrosis after MI/R. Transthoracic echocardiography was performed on MnSOD-overexpressing and wild-type mice that were subjected to a more prolonged period of reperfusion. Cardiac output was significantly depressed in the nontransgenic but not the transgenic MnSOD-treated mice. Anterior wall motion was significantly impaired in the nontransgenic mice. These findings demonstrate an important role for MnSOD but not Cu/ZnSOD or glutathione peroxidase in mice after in vivo MI/R.

scholarly journals Influence of dibornol-HES on electrophysiological parameters in the period of restoration of blood flow in rabbit myocardium

2018 ◽  
Vol 17 (4) ◽  
pp. 6-15
Author(s):  
M. A. Vaykshnorayte ◽  
V. A. Vityazev ◽  
N. A. Vahnina ◽  
V. D. Shadrina ◽  
M. A. Torlopov ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Occlusion ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Water Soluble ◽  
Control Group ◽  
Acute Ischemia ◽  
30Th Minute ◽  
Dispersion Of Repolarization ◽  
Experimental Group

Objective. Dibornol-HES, a water-soluble drug based on the derivative of 2,6-diisobornyl-4-methylphenol Dibornol conjugated with hydroxyethyl starch, can reduce the occurrence and severity of arrhythmias by preventive intravenous administration, but it is unknown whether the drug could reduce the myocardial arrhythmogenicity once ischemia has developed at the developed ischemia.Materials and methods. In the model of acute ischemia / reperfusion of the rabbit heart, the effect of Dibornol-HEC (80 mg/kg body weight of the animal) on the electrophysiological indices characterizing myocardial arrhythmogenicity (global and border dispersion of repolarization) was studied during the restoration of blood flow. In the model of acute ischemia / reperfusion with 64 unipolar epicardial leads, the activation-recovery intervals were measured and global and border dispersion of repolarization in the native rabbits (control group, n = 9) and in the rabbits treated by Dibornol-HES (on the 25th minute of occlusion, the experimental group, n = 6).Results. The introduction of Dibornol-HES did not lead to a change in the electrocardiographic parameters of rabbits. By the 30th minute of the coronary occlusion on the ECG in the animals of the control and the experimental groups, the intervals RR, QT, QTc were shortened (p < 0.05). In the animals of both groups by the 30th minute of coronary occlusion, the global dispersion of repolarization increased (p < 0.05), the boundary dispersion of repolarization also increased (p < 0.05), due to the decrease in the duration of the activation-recovery intervals in the ischemic zone (p < 0.05). During the 30-minute reperfusion the magnitude of the global dispersion of repolarization did not change in animals of the both groups, and the magnitude of the border dispersion of repolarization in the control rabbits decreased (p < 0.05), while in the rabbits treated by Dibornol-HES the border dispersion of repolarization did not changed.Conclusion. In rabbits of the experimental group, the values of the global and border dispersions of repolarization did not differ from those of the animals in the control group. Therefore, the administration to Dibornol-HES just prior to reperfusion does not lead to the decrease in the dispersion of repolarization increased as a result of acute ischemic myocardial damage.

Abstract 327: Apelin-13 Increases Myocardial Progenitor Cells and Improves Myocardial Remodeling of Post-myocardial Infarction.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
lanfang Li ◽  
Heng Zeng ◽  
Jian-Xiong Chen
Keyword(s):  
Myocardial Infarction ◽  
Progenitor Cells ◽  
Cardiac Remodeling ◽  
Cardiac Fibrosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cxcr4 Expression ◽  
Post Myocardial Infarction ◽  
Coronary Artery Ligation ◽  
Vascular Progenitor Cells

ABSTRACT: Apelin is an endogenous ligand for the angiotensin-like 1 receptor (APJ) and has beneficial effects against hypertension and myocardial ischemia/reperfusion injury. Little is known about the role of apelin in the homing of vascular progenitor cells (PCs) and cardiac remodeling post-myocardial infarction (MI). The present study investigates whether apelin affects PCs homing to the infarcted myocardium thereby mediating cardiac remodeling post-MI. Mice were infarcted by coronary artery ligation and apelin-13 (1 mg/kg.d) was injected for three days prior to MI and for either 24 hours or 14 days post MI. Homing of vascular progenitor cell (CD133 + /c-kit + /Sca1 + , CD133 + /SDF-1α + and CD133 + /CXCR4 + ) into the ischemic area were examined at 24 hours and 14 days post-MI. Myocardial Akt, eNOS, VEGF, Jagged1, Notch3, SDF-1α and CXCR4 expression were assessed. Functional analyses were performed at day 14 after MI. Mice receiving apelin-13 treatment demonstrated upregulation of SDF-1α/CXCR4 expression and dramatically increased the number of CD133 + /c-kit + /Sca1 + , CD133 + /SDF-1α + and c-kit + /CXCR4 + cells in the infarcted hearts. Apelin-13 also significantly increased Akt and eNOS phosphorylation and upregulated VEGF, Jagged1, Notch3 expression in the ischemic hearts. This was accompanied by a significant reduction of myocardial apoptosis. Further, treatment with apelin-13 promoted myocardial angiogenesis, attenuated cardiac fibrosis and hypertrophy together with a significant improvement of cardiac function at 14 days post-MI mice. Apelin-13 increases angiogenesis and improves cardiac remodeling by a mechanism involving upregulation of SDF-1α/CXCR4 and homing of vascular progenitor cells.

scholarly journals Swiprosin-1/EFhD-2 Expression in Cardiac Remodeling and Post-Infarct Repair: Effect of Ischemic Conditioning

2020 ◽  
Vol 21 (9) ◽  
pp. 3359
Author(s):  
Zoltán Giricz ◽  
András Makkos ◽  
Rolf Schreckenberg ◽  
Jochen Pöling ◽  
Holger Lörchner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Remodeling ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Common Mechanism ◽  
Structural Adaptation ◽  
Infarct Zone ◽  
Rat Cardiomyocytes ◽  
Ischemic Conditioning

Swiprosin-1 (EFhD2) is a molecule that triggers structural adaptation of isolated adult rat cardiomyocytes to cell culture conditions by initiating a process known as cell spreading. This process mimics central aspects of cardiac remodeling, as it occurs subsequent to myocardial infarction. However, expression of swiprosin-1 in cardiac tissue and its regulation in vivo has not yet been addressed. The expression of swiprosin-1 was analyzed in mice, rat, and pig hearts undergoing myocardial infarction or ischemia/reperfusion with or without cardiac protection by ischemic pre- and postconditioning. In mouse hearts, swiprosin-1 protein expression was increased after 4 and 7 days in myocardial infarct areas specifically in cardiomyocytes as verified by immunoblotting and histology. In rat hearts, swiprosin-1 mRNA expression was induced within 7 days after ischemia/reperfusion but this induction was abrogated by conditioning. As in cultured cardiomyocytes, the expression of swiprosin-1 was associated with a coinduction of arrestin-2, suggesting a common mechanism of regulation. Rno-miR-32-3p and rno-miR-34c-3p were associated with the regulation pattern of both molecules. Moreover, induction of swiprosin-1 and ssc-miR-34c was also confirmed in the infarct zone of pigs. In summary, our data show that up-regulation of swiprosin-1 appears in the postischemic heart during cardiac remodeling and repair in different species.

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