scholarly journals Role of PMN elastase on ischemic myocardial injury in evolving myocardial infarction: Correlation with clinical parameters and intervention by protease inhibitor ulinastatin.

1989 ◽  
Vol 53 (9) ◽  
pp. 1144-1151 ◽  
Author(s):  
SHINICHIRO SHIMAI ◽  
TERUO TAKANO ◽  
YOSHIHIKO SEINO ◽  
KEIJI TANAKA ◽  
HIROKAZU HAYAKAWA
Keyword(s):  
Myocardial Infarction ◽  
Protease Inhibitor ◽  
Myocardial Injury ◽  
Clinical Parameters ◽  
Pmn Elastase ◽  
Pmn Élastase

scholarly journals Neutrophil Elastase Deficiency Ameliorates Myocardial Injury Post Myocardial Infarction in Mice

2021 ◽  
Vol 22 (2) ◽  
pp. 722
Author(s):  
Yukino Ogura ◽  
Kazuko Tajiri ◽  
Nobuyuki Murakoshi ◽  
DongZhu Xu ◽  
Saori Yonebayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Neutrophil Elastase ◽  
Myocardial Injury ◽  
Flow Cytometric Analysis ◽  
Akt Signaling ◽  
Border Zone ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Deficient Mice

Neutrophils are recruited into the heart at an early stage following a myocardial infarction (MI). These secrete several proteases, one of them being neutrophil elastase (NE), which promotes inflammatory responses in several disease models. It has been shown that there is an increase in NE activity in patients with MI; however, the role of NE in MI remains unclear. Therefore, the present study aimed to investigate the role of NE in the pathogenesis of MI in mice. NE expression peaked on day 1 in the infarcted hearts. In addition, NE deficiency improved survival and cardiac function post-MI, limiting fibrosis in the noninfarcted myocardium. Sivelestat, an NE inhibitor, also improved survival and cardiac function post-MI. Flow cytometric analysis showed that the numbers of heart-infiltrating neutrophils and inflammatory macrophages (CD11b+F4/80+CD206low cells) were significantly lower in NE-deficient mice than in wild-type (WT) mice. At the border zone between intact and necrotic areas, the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive apoptotic cells was lower in NE-deficient mice than in WT mice. Western blot analyses revealed that the expression levels of insulin receptor substrate 1 and phosphorylation of Akt were significantly upregulated in NE-knockout mouse hearts, indicating that NE deficiency might improve cardiac survival by upregulating insulin/Akt signaling post-MI. Thus, NE may enhance myocardial injury by inducing an excessive inflammatory response and suppressing Akt signaling in cardiomyocytes. Inhibition of NE might serve as a novel therapeutic target in the treatment of MI.

scholarly journals Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Zheliang Zhou ◽  
Shuning Zhang ◽  
Suling Ding ◽  
Mieradilijiang Abudupataer ◽  
Zhiwei Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Apolipoprotein E ◽  
Myocardial Injury ◽  
Early Stage ◽  
Critical Role ◽  
Neutrophil Extracellular Trap ◽  
Coronary Artery Ligation ◽  
Infarct Zone ◽  
Dependent Pathway

Genetically human apolipoprotein E (APOE) ε32 is associated with a decreased risk of ischemic heart disease. ApoE deficiency in mice impairs infarct healing after myocardial infarction (MI). After the ischemic injury, a large number of neutrophils are firstly recruited into the infarct zone and then degrade dead material and promote reparative phase transformation. The role of ApoE in inflammation response in the early stage of MI remains largely unclear. In this study, we investigated the effect of ApoE deficiency on neutrophils’ function and myocardial injury after myocardial infarction. By left coronary artery ligation in ApoE-/- and wild-type (WT) mice, we observed increased infarct size and neutrophil infiltration in ApoE-/- mice. Within the infarct zone, more neutrophil extracellular traps (NETs) were observed in ApoE-/- mice, while increased ex vivo NET formation was detected in ApoE-/- mouse-derived neutrophils through the NADPH oxidase-ROS-dependent pathway. Suppressing overproduced NETs reduced myocardial injury in ApoE-/- mice after ligation. In general, our findings reveal a critical role of apolipoprotein E in regulating Ly6G+ neutrophil activation and NET formation, resulting in limiting myocardial injury after myocardial infarction. In such a process, apolipoprotein E regulates NET formation via the ROS-MAPK-MSK1 pathway.

scholarly journals Inflammation in myocardial injury: mesenchymal stem cells as potential immunomodulators

2019 ◽  
Vol 317 (2) ◽  
pp. H213-H225 ◽  
Author(s):  
Weiang Yan ◽  
Ejlal Abu-El-Rub ◽  
Sekaran Saravanan ◽  
Lorrie A. Kirshenbaum ◽  
Rakesh C. Arora ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Significant Risk ◽  
Secondary Injury ◽  
Irreversible Loss ◽  
Mesenchymal Stem Cell Therapy ◽  
Number Of Patients ◽  
Adverse Remodeling

Ischemic heart disease is a growing worldwide epidemic. Improvements in medical and surgical therapies have reduced early mortality after acute myocardial infarction and increased the number of patients living with chronic heart failure. The irreversible loss of functional cardiomyocytes puts these patients at significant risk of ongoing morbidity and mortality after their index event. Recent evidence suggests that inflammation is a key mediator of postinfarction adverse remodeling in the heart. In this review, we discuss the cardioprotective and deleterious effects of inflammation and its mediators during acute myocardial infarction. We also explore the role of mesenchymal stem cell therapy to limit secondary injury and promote myocardial healing after myocardial infarction.

MYOCARDIAL INFARCTION WITH NONOBSTRUCTIVE CORONARY ATHEROSCLEROSIS AS A CURRENT PROBLEM OF EMERGENCY CARDIOLOGY

2019 ◽  
Vol 33 (4) ◽  
pp. 10-18 ◽  
Author(s):  
V. V. Ryabov ◽  
S. B. Fedorova ◽  
E. V. Vyshlov
Keyword(s):  
Myocardial Infarction ◽  
Coronary Atherosclerosis ◽  
Myocardial Injury ◽  
Current Problem ◽  
Diagnostic Algorithm ◽  
Future Research ◽  
Resonance Imaging ◽  
Definition Of ◽  
A Current

Myocardial infarction with nonobstructive coronary atherosclerosis is a term which emerged recently, but it is of great importance for current clinical practice. Under the mask of this diagnosis, not only ischemia-caused myocardial infarction is hiding, but also diseases with alternative mechanisms of myocardial injury. This review presents a definition of this term as well as differential diagnostic algorithm for diseases associated with increase in the myocardial injury markers. The role of magnetic resonance imaging is emphasized as it is the key method for diagnosis of cardiac diseases. Main principles of current recommendations in this regard are presented. Unsolved and undeveloped aspects of this problem are discussed. Directions for future research are outlined.

scholarly journals MicroRNA-322-5p Protects Against Myocardial Infarction through Targeting BTG2

2021 ◽  
Author(s):  
Yang Ruan ◽  
Shuai Meng ◽  
Ruofei Jia ◽  
Xiaojing Cao ◽  
zening Jin
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
B Cell ◽  
Rat Model ◽  
Myocardial Injury ◽  
Pathological Condition ◽  
Current Paper ◽  
Targeted Treatment ◽  
Myocardial Tissue

Abstract Objective: A large cohort of studies have addressed the therapeutic importance of microRNA (miR) in the treatment of myocardial infarction (MI). The current paper gives prominence to the role of miR-322-5p in MI by regulating B-cell translocation gene 2 (BTG2).Methods: In a rat model of MI miR-322-5p and BTG2 expression was estimated. Adenovirus that altered miR-322-5p or BTG2 expression was injected into MI rats. After that, cardiac function, inflammation, myocardial injury, pathological condition, apoptosis, and the NF-κB pathway-related genes in the myocardial tissue of MI rats after targeted treatment were evaluated. The targeting relationship between miR-322-5p and BTG2 was assessed.Results: miR-322-5p was lowly expressed and BTG2 was highly expressed in the myocardial tissue of MI rats. Restored miR-322-5p improved cardiac function, relived inflammation and myocardial injury, suppressed pathological condition and apoptosis and inactivated NF-κB pathway in MI rats. BTG2 expression was negatively mediated by miR-322-5p. Overexpressed BTG2 rescued miR-322-5p-induced cardioprotection on MI rats.Conclusion: It is evident that miR-322-5p protects against MI through suppressing BTG2 expression.

scholarly journals Upregulated microRNA-210-3p Improves Sevoflurane-induced Protective Effect on Ventricular Remodeling in Rats With Myocardial Infarction by Inhibiting ADCY9

2021 ◽  
Author(s):  
Yahui Wu ◽  
Taofu Wang ◽  
Liang Qiao ◽  
Hongqi Lin
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Protective Effect ◽  
Adenylyl Cyclase ◽  
Cause Of Death ◽  
Myocardial Injury ◽  
Ventricular Remodeling ◽  
Cardiomyocyte Apoptosis

Abstract ObjectiveMyocardial infarction (MI) is a significant cause of death and disability, and sevoflurane (sevo) can protect myocardium in clinic. We aim to assess the effects of miR-210-3p on MI rats undergoing sevo treatment with the involvement of adenylyl cyclase type 9 (ADCY9).MethodsRat MI models were constructed by ligation of the left anterior descending and the modeled mice were respectively treated with sevo, miR-210-3p agomir/antagomir or overexpressed ADCY9. Then, miR-210-3p and ADCY9 expression, cardiac function, myocardial injury and fibrosis, and cardiomyocyte apoptosis in rats were evaluated. Target relation between miR-210-3p and ADCY9 was detected.ResultsMiR-210-3p was downregulated while ADCY9 was upregulated in MI rats. Sevo was able to promote cardiac function and attenuate myocardial injury and fibrosis, as well as cardiomyocyte apoptosis in MI rats. These effects of sevo were strengthened by miR-210-3p elevation while abolished by miR-210-3p inhibition. The role of elevated miR-210-3p in MI rats was reversed by overexpression of ADCY9.ConclusionUpregulated miR-210-3p improves sevo-induced protective effect on ventricular remodeling in rats with MI through inhibiting ADCY9.

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