scholarly journals 0375: Re-evaluation of the role of mast cell in cardiac tissue following myocardial infarction

Author(s):  
Anta Ngkelo ◽  
Adele Richart ◽  
Jose Vilar ◽  
Pauline Marck ◽  
Christophe Heymes ◽  
...  
2014 ◽  
Vol 458 (2) ◽  
pp. 187-193 ◽  
Author(s):  
María Fernández-Velasco ◽  
Silvia González-Ramos ◽  
Lisardo Boscá

Emerging evidence points to the involvement of specialized cells of the immune system as key drivers in the pathophysiology of cardiovascular diseases. Monocytes are an essential cell component of the innate immune system that rapidly mobilize from the bone marrow to wounded tissues where they differentiate into macrophages or dendritic cells and trigger an immune response. In the healthy heart a limited, but near-constant, number of resident macrophages have been detected; however, this number significantly increases during cardiac damage. Shortly after initial cardiac injury, e.g. myocardial infarction, a large number of macrophages harbouring a pro-inflammatory profile (M1) are rapidly recruited to the cardiac tissue, where they contribute to cardiac remodelling. After this initial period, resolution takes place in the wound, and the infiltrated macrophages display a predominant deactivation/pro-resolution profile (M2), promoting cardiac repair by mediating pro-fibrotic responses. In the present review we focus on the role of the immune cells, particularly in the monocyte/macrophage population, in the progression of the major cardiac pathologies myocardial infarction and atherosclerosis.


2019 ◽  
Vol 19 (17) ◽  
pp. 1407-1426 ◽  
Author(s):  
Khairul Anwar Zarkasi ◽  
Tan Jen-Kit ◽  
Zakiah Jubri

: Myocardial infarction is a major cause of deaths globally. Modulation of several molecular mechanisms occurs during the initial stages of myocardial ischemia prior to permanent cardiac tissue damage, which involves both pathogenic as well as survival pathways in the cardiomyocyte. Currently, there is increasing evidence regarding the cardioprotective role of vitamin E in alleviating the disease. This fat-soluble vitamin does not only act as a powerful antioxidant; but it also has the ability to regulate several intracellular signalling pathways including HIF-1, PPAR-γ, Nrf-2, and NF-κB that influence the expression of a number of genes and their protein products. Essentially, it inhibits the molecular progression of tissue damage and preserves myocardial tissue viability. This review aims to summarize the molecular understanding of the cardiomodulation in myocardial infarction as well as the mechanism of vitamin E protection.


2017 ◽  
Vol 66 (9) ◽  
pp. 739-751 ◽  
Author(s):  
Arman Saparov ◽  
Vyacheslav Ogay ◽  
Talgat Nurgozhin ◽  
William C. W. Chen ◽  
Nurlan Mansurov ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jinli Wang ◽  
Wanqing Sun ◽  
George Techiryan ◽  
Frederick Sachs ◽  
Thomas Suchyna ◽  
...  

Introduction: Reperfusion of ischemic cardiac tissue by percutaneous coronary intervention has become a routine treatment for acute ST-elevation myocardial infarction. However, restoring blood flow to ischemic cardiac tissue can injure myocytes that were viable prior to reperfusion. The putative causes of ischemia/reperfusion (I/R) injury are varied, though cation imbalance has long been known to be a significant contributor. GsMTx4 peptide is a selective inhibitor of cation selective mechanosensitive ion channels (MSCs) and has helped establish the role of MSCs in cardiac physiology. However, the role of MSCs in ischemic reperfusion injury remain uncertain. Hypothesis: Pathological stresses from swelling and hypercontracture during I/R can activate cationic MSCs, the D enantiomer of GsMTx4 can act as a cardioprotectant during I/R. Methods: GsMTx4-D pharmacokinetics in the plasma and heart was monitored over 24 h using an LCMSMS assay. The cardioprotective activities of GsMTx4 were monitored in a mouse model of ischemia/reperfusion (I/R) injury in which the left anterior descending coronary artery (LAD) was occluded and then released. The influence of GsMTx4 on contractile function and transient calcium signaling of cardiomyocyte were assessed by SoftEdge MyoCam system. Results: GsMTx4-D reduced infarct area by >40% for both acute and pretreated animals relative to vehicle injected animals (p<0.01). Cardiac output was significantly improved in GsMTx4-D pretreatment group, and arrhythmias were also significantly reduced by intravenous injections of GsMTx4-D. The further studies with isolated cardiomyocytes revealed that GsMTx4-D improved contractility and intracellular transient calcium signaling of cardiomyocytes under hypoxia/reoxygenation conditions. The immunoblotting data demonstrated that administration of GsMTx4-D attenuated I/R-induced inflammatory c-Jun N-terminal protein kinase (JNK) and NF-κB signaling pathways in the hearts. Conclusions: GsMTx4-D is a potent cardioprotectant that decreases infarct area, improves heart function, reduces arrhythmias and attenuates inflammatory signaling pathways that are caused by I/R. Thus GsMTx4-D could be a useful therapy in treating cardiac I/R injury.


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