scholarly journals LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2

Cell Cycle ◽  
2019 ◽  
Vol 18 (23) ◽  
pp. 3393-3403 ◽  
Author(s):  
Jinhua Yang ◽  
Xianwei Huang ◽  
Fudong Hu ◽  
Xin Fu ◽  
Zhengming Jiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cell Apoptosis ◽  
Myocardial Cell

scholarly journals Knockdown of circROBO2 attenuates acute myocardial infarction through regulating the miR-1184/TRADD axis

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Tian-ping Chen ◽  
Nai-ju Zhang ◽  
Hong-ju Wang ◽  
Si-gan Hu ◽  
Xu Geng
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cell Apoptosis ◽  
Myocardial Cell ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Luciferase Reporter Gene ◽  
Expression Levels ◽  
Creatine Kinase Mb

Abstract Background Studies have found that circular RNAs (circRNAs) play key roles in cardiovascular diseases. However, the function of circROBO2 in acute myocardial infarction (AMI) is unclear. This study aimed to investigate the pathogenesis of circROBO2 in AMI. Methods qRT-PCR and Western blot were used to determine the expression levels of circROBO2, miR-1184, and TRADD in AMI and sham-operated mouse models at mRNA and protein level, respectively. The relationship among miR-1184, circROBO2 and TRADD was evaluated by RNA immunoprecipitation (RIP) analysis and luciferase reporter gene analysis. The roles of circROBO2, miR-1184, and TRADD in myocardial cell apoptosis were evaluated using flow cytometry. Ultrasound echocardiography, serum creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarction area, and myocardial cell apoptosis were measured to examine the effects of circROBO2 on myocardial injury. Results The expression levels of miR-1184 were significantly reduced, and the expression levels of circROBO2 and TRADD were significantly increased in MI group. CircROBO2 acted as a sponge for miR-1184 by upregulating the expression of TRADD. In addition, overexpression of miR-1184 enhanced the protective effect of knockdown of circROBO2 by partially inhibiting the expression of TRADD in vivo and in vitro. Conclusion Knockdown of circROBO2 reduced the apoptosis of cardiomyocytes by increasing the expression levels of miR-1184, which in turn decreased the expression levels of TRADD in the myocardium post-MI.

scholarly journals RGD-PEG-PLA Delivers MiR-133 to Infarct Lesions of Acute Myocardial Infarction Model Rats for Cardiac Protection

Pharmaceutics ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 575 ◽  
Author(s):  
Bixi Sun ◽  
Shuwen Liu ◽  
Rubin Hao ◽  
Xinyue Dong ◽  
Lanbo Fu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Disease Model ◽  
Adenosine Monophosphate ◽  
Myocardial Cell ◽  
Protective Role ◽  
Cardiac Protection ◽  
Multiple Perspectives ◽  
Positive Role

Studies have shown that microRNA-133 (miR-133) plays a positive role in the growth of cardiac myocytes, the maintenance of cardiac homeostasis, and the recovery of cardiac function, which is of great significance for the recovery of acute myocardial infarction. However, the delivery of miRNA to the site of action remains a challenge at present. The purpose of this study was to design an ideal carrier to facilitate the delivery of miR-133 to the infarct lesion for cardiac protection. A disease model was constructed by ligating the left anterior descending coronary artery of rats, and polyethylene glycol (PEG)-polylactic acid (PLA) nanoparticles modified with arginine-glycine-aspartic acid tripeptide (RGD) carrying miR-133 were injected via the tail vein. The effects of miR-133 were evaluated from multiple perspectives, including cardiac function, blood indexes, histopathology, and myocardial cell apoptosis. The results showed that RGD-PEG-PLA maintained a high level of distribution in the hearts of model rats, indicating the role of the carrier in targeting the heart infarction lesions. RGD-PEG-PLA/miR-133 alleviated cardiac histopathological changes, reduced the apoptosis of cardiomyocytes, and reduced the levels of factors associated with myocardial injury. Studies on the mechanism of miR-133 by immunohistochemistry and polymerase chain reaction demonstrated that the expression level of Sirtuin3 (SIRT3) was increased and that the expression of adenosine monophosphate activated protein kinase (AMPK) decreased in myocardial tissue. In summary, the delivery of miR-133 by RGD-PEG-PLA carrier can achieve cardiac lesion accumulation, thereby improving the cardiac function damage and reducing the myocardial infarction area. The inhibition of cardiomyocyte apoptosis, inflammation, and oxidative stress plays a protective role in the heart. The mechanism may be related to the regulation of the SIRT3/AMPK pathway.

scholarly journals How to Use High-Sensitivity Cardiac Troponins in Acute Cardiac Care?

2013 ◽  
Vol 2013 ◽  
pp. 1-4
Author(s):  
H. Katus ◽  
J. Searle ◽  
E. Giannitsis
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
High Sensitivity ◽  
Myocardial Cell ◽  
Significant Rise ◽  
Specific Detection ◽  
Great Chance ◽  
Patients At Risk ◽  
Diagnostic Benefit ◽  
Rule Out

High-sensitivity troponin assays, when used and viewed in the clinical context, provide a definite diagnostic benefit compared to conventional troponin assays, especially due to the improved early rule-out of acute myocardial infarction in troponin-negative patients. The interpretation of positive troponin results and, thus, the rule-in of acute myocardial infarction have become more challenging. High sensitivity Tn assays can detect very small but prognostically significant troponin increases, but the underlying diagnoses are diverse. Especially patients with non-ACS-related troponin elevations have an adverse outcome and require careful patient management. Additionally, the interpretation of a significant rise or fall of troponin values has not been standardized yet. Despite these challenges, troponin is a unique marker, which allows for the specific detection of myocardial cell necrosis and the new high sensitivity assays are a great chance to identify more patients at risk and improve their management and care.

Platelet Function Changes In Acute Myocardial Infarction

1981 ◽  
Author(s):  
A Strano ◽  
A Raineri ◽  
S Novo ◽  
G L Piraino ◽  
A Mazzola ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Function ◽  
Regional Blood Flow ◽  
Coronary Artery Spasm ◽  
Myocardial Cell ◽  
Thromboxane B2 ◽  
Time Interval ◽  
Additional Mechanism ◽  
Local Release

Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanism from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Recently in some cases of infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet-aggregating substances, are released by platelets during myocardial ischemia. The local release of these substances may modify the myocardial cell viability and regional blood flow.The aim of the present study was to investigate changes in platelet function in relation to the time interval after the beginning of the chest pain in 8 patients suffering from acu te myocardial infarction.The following parameters were estimated: plasmatic PF4 and BTG levels, thromboxane B2 formation by platelets stimulated with thrombin, plasmatic levels of thromboxane B2 MDA formation by platelets stimulated with thrombin, platelet sensi tivity to exogenous prostacyclin; factor XIII activity was also determined.The tests showed, in the first three days, an augmented re lease of platelet constituents together with a “platelet exhaustion”, demonstrated by a reduced formation of MDA and thromboxane B2; in the following days the platelets changed to a state of hyperactivity. The platelet sensitivity to pro stacyclin was reduced during the whole period after the onset of the acute myocardial infarction; this provides an additional mechanism involved in increased platelet aggregation.

MiR-128/SOX7 alleviates myocardial ischemia injury by regulating IL-33/sST2 in acute myocardial infarction

2019 ◽  
Vol 400 (4) ◽  
pp. 533-544 ◽  
Author(s):  
Jinhua Yang ◽  
Fudong Hu ◽  
Xin Fu ◽  
Zhengming Jiang ◽  
Wencai Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cell Apoptosis ◽  
Human Life ◽  
Luciferase Reporter ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Polymerase Chain ◽  
The Relationship

Abstract Acute myocardial infarction (AMI) induced by ischemia hypoxia severely threatens human life. Cell apoptosis of neurocytes was identified to mediate the pathogenesis, while the potential mechanism was still unclear. Sprague Dawley (SD) rats were used to establish the AMI rat model. Real-time polymerase chain reaction (PCR) and Western blot were performed to detect gene expression in mRNA and protein levels, respectively. A TUNEL assay was carried out to determine cell apoptosis. The relationship between SRY-related HMG-box (SOX7) and miR-128 was verified using luciferase reporter assay. The expression of SOX7 was decreased, while miR-128 was increased in AMI rats and ischemia hypoxia (IH) induced H9c2 cells. Hypoxia induction significantly promoted the expression of interleukin (IL)-33 and soluble ST2 (sST2), and also promoted cell apoptosis. MiR-128 targets SOX7 to regulate its expression. Down-regulated miR-128 reversed the effects of IH on expression of SOX7, sST2 and cell apoptosis, while down-regulated sST2 abolished the effects of miR-128 inhibitor. In addition, overexpressed IL-33 abolished the effects of miR-128 inhibitor that induced by IH on the expression of SOX7 and cell apoptosis. In vivo experiments validated the expression of miR-128 on cell apoptosis. The present study indicated that miR-128 modulated cell apoptosis by targeting SOX7, which was mediated by IL-33/sST2 signaling pathway.

Prevention of endothelial cell apoptosis induced by neutrophils and sera from patients with acute myocardial infarction

2010 ◽  
Vol 144 (1) ◽  
pp. 151-154 ◽  
Author(s):  
Silvius Frimmel ◽  
Christoph Josef Hemmer ◽  
Jana Kenzler ◽  
Marcus Unverricht ◽  
Hüseyin Ince ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis

scholarly journals Serum magnesium level and QTc interval prolongation in acute myocardial infarction patients and its correlation with arrhythmias

2019 ◽  
Vol 7 (11) ◽  
pp. 4015
Author(s):  
Laxmi Mohanani ◽  
Kuldeep Deopujari ◽  
Rangvendra Singh Meena ◽  
T. N. Dubey
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Serum Magnesium ◽  
Myocardial Cell ◽  
Magnesium Level ◽  
Qtc Interval ◽  
Serum Magnesium Level ◽  
Interval Prolongation ◽  
Low Magnesium ◽  
Qtc Interval Prolongation

Background: Arrhythmias commonly occur early in acute myocardial infarction and remain a common cause of sudden death in AMI. Magnesium has been implicated in the pathogenesis of acute myocardial infarction and its complication like arrhythmia. Magnesium improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death. It improves vascular tone, peripheral vascular resistance, after load and cardiac output and reduces cardiac arrhythmias. The objective of this study to investigate the serum magnesium level and QTc interval prolongation in AMI and its correlation with arrhythmias.Methods: In this study, 200 patients of AMI were enrolled. ECG and cardiac parameters were examined. Serum magnesium level is measured and the QTc interval was calculated.Results: MI was more prevalent in the male patients (63.3%) and age group of 41-50 years. Hypertension (35.7%), smoking (34.2%), and diabetes (23.1%) were the major risk factor for MI. Mean serum magnesium level was 1.64±0.37 among those having arrhythmia that is significantly low as compared to those having no arrhythmia among which mean serum magnesium level was 2.28±0.31 (p<0.001). Mean QTc was higher (546.88 ms vs. 404.33ms) in patients documented with arrhythmia compared with those who had no arrhythmia (p<0.001).Conclusions: In acute myocardial infarction, patients with low magnesium levels and prolonged QTc interval are more prone to get arrhythmias. So magnesium treatment can be considered in patients of acute myocardial infarction with low magnesium levels.

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