Reduced Histone Deacetylase 3 Attenuates Cardiac Microvascular Endothelial Cell Injury after Myocardial Ischemia-Reperfusion Injury by Elevating microRNA-17-3p and Inhibiting Cylindromatosis

2020 ◽  
Author(s):  
Yu Wang ◽  
Dong Zhen ◽  
Dan-Ni Fu ◽  
Guo-Hua Gong ◽  
Li-Jun Yu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Injury ◽  
Histone Deacetylase 3 ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Cardiac Microvascular Endothelial Cell

scholarly journals Endothelial Cell Cystathionine γ‐Lyase Expression Level Modulates Exercise Capacity, Vascular Function, and Myocardial Ischemia Reperfusion Injury

2020 ◽  
Vol 9 (19) ◽  
Author(s):  
Huijing Xia ◽  
Zhen Li ◽  
Thomas E. Sharp ◽  
David J. Polhemus ◽  
Jean Carnal ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Reperfusion Injury ◽  
Exercise Capacity ◽  
Vascular Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Genetic Deletion ◽  
Myocardial Ischemia Reperfusion

Background Hydrogen sulfide (H 2 S) is an important endogenous physiological signaling molecule and exerts protective properties in the cardiovascular system. Cystathionine γ‐lyase (CSE), 1 of 3 H 2 S producing enzyme, is predominantly localized in the vascular endothelium. However, the regulation of CSE in vascular endothelium remains incompletely understood. Methods and Results We generated inducible endothelial cell‐specific CSE overexpressed transgenic mice (EC‐CSE Tg) and endothelial cell‐specific CSE knockout mice (EC‐CSE KO), and investigated vascular function in isolated thoracic aorta, treadmill exercise capacity, and myocardial injury following ischemia‐reperfusion in these mice. Overexpression of CSE in endothelial cells resulted in increased circulating and myocardial H 2 S and NO, augmented endothelial‐dependent vasorelaxation response in thoracic aorta, improved exercise capacity, and reduced myocardial‐reperfusion injury. In contrast, genetic deletion of CSE in endothelial cells led to decreased circulating H 2 S and cardiac NO production, impaired endothelial dependent vasorelaxation response and reduced exercise capacity. However, myocardial‐reperfusion injury was not affected by genetic deletion of endothelial cell CSE. Conclusions CSE‐derived H 2 S production in endothelial cells is critical in maintaining endothelial function, exercise capacity, and protecting against myocardial ischemia/reperfusion injury. Our data suggest that the endothelial NO synthase—NO pathway is likely involved in the beneficial effects of overexpression of CSE in the endothelium.

Treating myocardial ischemia-reperfusion injury by targeting endothelial cell transcription

1999 ◽  
Vol 68 (5) ◽  
pp. 1949-1953 ◽  
Author(s):  
Edward M Boyle ◽  
Timothy G Canty ◽  
Elizabeth N Morgan ◽  
Wang Yun ◽  
Timothy H Pohlman ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Endothelial Cell Injury in Cardiovascular Surgery: The Systemic Inflammatory Response11Recent discoveries in the field of vascular biology have led to an expanded understanding of the pathogenesis of many of the immediate and long-term complications of patients undergoing cardiovascular operations and interventional cardiologic procedures. In particular, the vascular endothelium has emerged as the central focus of many of the biologic events that affect the preoperative, operative, and postoperative course of nearly all heart surgery patients. A recurring theme in the study of endothelial cell biology is the crucial role that endothelial cell injury plays in the difficulties that our patients encounter. The deleterious effects of endothelial cell injury are most evident in the acute syndromes of vasospasm, coagulopathy, ischemia/reperfusion injury, and the systemic inflammatory response to cardiopulmonary bypass. In addition, chronic endothelial cell injury contributes to the development of anastomotic narrowing and the progression of atherosclerosis, both of which limit the long-term success of coronary artery bypass grafting. Because of the increasingly recognized role of the endothelium in cardiovascular function there is a tremendous amount of basic science information detailing the response of the endothelium to injury. This is the fifth in a series of seven reviews intended as an introduction to the major topics of endothelial cell biology that are of importance to the practicing cardiothoracic surgeon. In particular, the authors have focused on the role that the endothelium has on the development of vasomotor dysfunction, bleeding and thrombosis, neutrophil-endothelial cell interaction, and obstructive arteriopathy. The aim of these reviews is to provide a concise reference point for cardiothoracic surgeons as they evaluate the ever-accumulating research findings and new therapies that stem from the study of the endothelium in response to the insults encountered in cardiothoracic surgery.Edward D. Verrier, MD

1997 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Edward M Boyle, MD ◽  
Timothy H Pohlman, MD ◽  
Marion C Johnson, MD ◽  
Edward D Verrier, MD
Keyword(s):  
Endothelial Cell ◽  
Cell Biology ◽  
Heart Surgery ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Cell Interaction ◽  
Endothelial Cell Injury

Non-carbonyl Curcuma longa [NCCL] protects the heart from myocardial ischemia/reperfusion injury by reducing endothelial microparticle mediated inflammation in rats

RSC Advances ◽  
2016 ◽  
Vol 6 (60) ◽  
pp. 54938-54948 ◽  
Author(s):  
Amit Manhas ◽  
Dipti Tripathi ◽  
Bharti Biswas ◽  
Hafsa Ahmad ◽  
Dipika Goyal ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Cell ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Curcuma Longa ◽  
Ischemia Reperfusion ◽  
Post Myocardial Infarction ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Endothelial cell mediated inflammation flags and mediates the progression of pre and post myocardial infarction.

Protective effect of Shengmai injection on myocardial endothelial cell glycoprotein detachment after myocardial ischemia-reperfusion injury in isolated rat hearts

Perfusion ◽  
2020 ◽  
pp. 026765912096592
Author(s):  
Qi Chen ◽  
Ping Zhang ◽  
Qiu-Xia Xiao ◽  
Qing Liu ◽  
Ying Zhang
Keyword(s):  
Endothelial Cell ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Stress Injury ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective: To investigate effects of Shengmai injection (SMI) postconditioning on myocardial ischemia-reperfusion injury (MIRI) in isolated rat hearts. Materials and methods: A total of thirty isolated hearts were randomly divided into three groups: Sham group, I/R group and SMI group. Sham group was continuously perfused with K-H solution for 120 minutes. I/R group and SMI group were given balanced perfusion for 30 min followed by reperfusion for 60 min, with an interval of 30 min, and those in the SMI group were given postconditioning with 1% SMI during the first 10 min of reperfusion. The left ventricular function, markers of myocardial injury, endothelial cell injury and oxidative stress injury were measured at 30 minutes after equilibration (t0), 30 minutes after ischemia (t2) and 60 minutes after reperfusion (t3). Results: The results showed that there was no significant difference for all observation indexes at t0. Compared with the Sham group, real portfolio project and coronary arterial flow rate and the activity of superoxide dismutase were significantly decreased in the I/R group, whereas those in the SMI group were significantly higher. Left ventricular end-diastolic pressure, the concentrate of malondialdehyde, lactate dehydrogenase, cTn-I, hyaluronic acid, heparin sulphate, syndecan-1 in the I/R group were markedly higher than those in the Sham group, whereas those in the SMI group were significantly lower. Conclusion: In summary, the present study indicated that 1% SMI postconditioning can alleviate the detachment of endothelial cell glycoprotein envelope induced by myocardial ischemia-reperfusion injury, and its mechanism is probably related to the inhibition of the oxidative stress injury.

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