scholarly journals Exosomes and myocardial infarction: scientific and practical interest

2021 ◽  
Vol 38 (4) ◽  
pp. 76-84
Author(s):  
O. V. Khlynova ◽  
R. A. Rodionov ◽  
N. S. Karpunina ◽  
E. A. Shishkina
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Practical Interest ◽  
Biological Information ◽  
Cardiac Damage ◽  
Intercellular Transport ◽  
Pathological Conditions ◽  
Damage Repair ◽  
Strong Inflammatory Response

A review of the literature on the biological role of exosomes in the pathophysiology of a number of pathological conditions, including damage to the heart muscle in the variant of myocardial infarction (MI), is presented. In the last decade, exosomes have begun to be actively studied; a lot of data have appeared on their nature and role in intercellular transport and signaling both in normal conditions and in pathology. Exosomes are important carriers of biological information, facilitating intercellular communication and participating in the pathophysiology of various cardiovascular diseases. In myocardial infarction, massive cardiomyocyte death triggers a strong inflammatory response, which is a vital process for cardiac damage, repair, and remodeling. A growing body of evidence suggests that exosomes are involved in the inflammatory response and immune regulation after MI.

Involvement of monocytes/macrophages as key factors in the development and progression of cardiovascular diseases

2014 ◽  
Vol 458 (2) ◽  
pp. 187-193 ◽  
Author(s):  
María Fernández-Velasco ◽  
Silvia González-Ramos ◽  
Lisardo Boscá
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Cardiovascular Diseases ◽  
Cardiac Tissue ◽  
Initial Period ◽  
Cardiac Injury ◽  
Key Factors ◽  
Cardiac Damage ◽  
Inflammatory Profile

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.

Effect of vitamin D on isoprenaline-induced myocardial infarction in rats: possible role of peroxisome proliferator-activated receptor-γ

2017 ◽  
Vol 95 (6) ◽  
pp. 641-646 ◽  
Author(s):  
Ola Ahmed El-Gohary ◽  
Mona Maher Allam
Keyword(s):  
Myocardial Infarction ◽  
Vitamin D ◽  
Diglycidyl Ether ◽  
Peroxisome Proliferator ◽  
Oxidative Stress Biomarkers ◽  
Cardiac Damage ◽  
Necrosis Factor Alpha ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ

Infarct-like lesion induced by isoprenaline is a well-known model to study myocardial infarction (MI). Vitamin D has been shown to have anti-inflammatory and antioxidant effects. Recent studies highlighted cross talk between vitamin D and peroxisome proliferator-activated receptor gamma (PPAR-γ). The present study was designed to investigate the effect of pretreatment with vitamin D on the isoprenaline-induced infarct-like lesion in rats and the role of PPAR-γ as a novel mechanism in vitamin-D-mediated cardioprotective effect. Markers chosen to assess cardiac damage included serum level of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Cardiac contents of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH) were also assessed. Furthermore, ECG monitoring and measurement of injury extension were carried out. Isoprenaline increased the level of cardiac enzymes, as well as inflammatory and oxidative stress biomarkers. In addition, it produced ST-segment elevation. Pretreatment with vitamin D significantly improved previous parameters. The prior treatment with bisphenol A diglycidyl ether (BADGE), a PPAR-γ antagonist, significantly attenuated the protective effect of vitamin D. In conclusion, vitamin D can be demonstrated as a promising cardioprotective agent in MI and PPAR-γ significantly contributes toward vitamin-D-mediated protection.

scholarly journals Role of Adrenomedullin in Lyme Disease

2010 ◽  
Vol 78 (12) ◽  
pp. 5307-5313 ◽  
Author(s):  
Meghan L. Marre ◽  
Courtney T. Darcy ◽  
Janeth Yinh ◽  
Shizuo Akira ◽  
Satoshi Uematsu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Lyme Arthritis ◽  
Signaling Cascades ◽  
Mammalian Host ◽  
Phosphatidylinositol 3 Kinase ◽  
Raw264.7 Macrophages ◽  
Osteoarthritis Patient ◽  
Strong Inflammatory Response

ABSTRACT Borrelia burgdorferi stimulates a strong inflammatory response during infection of a mammalian host. To understand the mechanisms of immune regulation employed by the host to control this inflammatory response, we focused our studies on adrenomedullin, a peptide produced in response to bacterial stimuli that exhibits antimicrobial activity and regulates inflammatory responses by modulating the expression of inflammatory cytokines. Specifically, we investigated the effect of B. burgdorferi on the expression of adrenomedullin as well as the ability of adrenomedullin to dampen host inflammatory responses to the spirochete. The concentration of adrenomedullin in the synovial fluid of untreated Lyme arthritis patients was elevated compared with that in control osteoarthritis patient samples. In addition, coculture with B. burgdorferi significantly increased the expression of adrenomedullin in RAW264.7 macrophages through MyD88-, phosphatidylinositol 3-kinase (PI3-K)-, and p38-dependent signaling cascades. Furthermore, the addition of exogenous adrenomedullin to B. burgdorferi-stimulated RAW264.7 macrophages resulted in a significant decrease in the induction of proinflammatory cytokines. Taken together, these results suggest that B. burgdorferi increases the production of adrenomedullin, which in turn negatively regulates the B. burgdorferi-stimulated inflammatory response.

scholarly journals Role of Exercise Training on Autonomic Changes and Inflammatory Profile Induced by Myocardial Infarction

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Bruno Rodrigues ◽  
Fabio S. Lira ◽  
Fernanda M. Consolim-Colombo ◽  
Juraci A. Rocha ◽  
Erico C. Caperuto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mortality Rate ◽  
Exercise Training ◽  
Autonomic Imbalance ◽  
Pathological Conditions ◽  
Autonomic Changes ◽  
Immunological Changes ◽  
Inflammatory Profile ◽  
Parasympathetic Function

The cardiovascular autonomic imbalance in patients after myocardial infarction (MI) provides a significant increase in mortality rate, and seems to precede metabolic, hormonal, and immunological changes. Moreover, the reduction in the parasympathetic function has been associated with inflammatory response in different pathological conditions. Over the years, most of the studies have indicated the exercise training (ET) as an important nonpharmacological tool in the management of autonomic dysfunction and reduction in inflammatory profile after a myocardial infarction. In this work, we reviewed the effects of ET on autonomic imbalance after MI, and its consequences, particularly, in the post-MI inflammatory profile. Clinical and experimental evidence regarding relationship between alterations in autonomic regulation and local or systemic inflammation response after MI were also discussed.

scholarly journals Role of Androgens in Sex Differences in Cardiac Damage During Myocardial Infarction

Endocrinology ◽  
2014 ◽  
Vol 155 (2) ◽  
pp. 568-575 ◽  
Author(s):  
Thi Y. L. Le ◽  
Anthony W. Ashton ◽  
Mahidi Mardini ◽  
Peter G. Stanton ◽  
John W. Funder ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sex Differences ◽  
Androgen Receptor ◽  
Sex Steroids ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
B Cell Lymphoma ◽  
Male Rats ◽  
Cardiac Damage

Age-specific incidence of ischemic heart disease in men is higher than in women, although women die more frequently without previous symptoms; the molecular mechanism(s) are poorly understood. Most studies focus on protection by estrogen, with less attention on androgen receptor-mediated androgen actions. Our aim was to determine the role of androgens in the sex differences in cardiac damage during myocardial infarction. Mature age-matched male and female Sprague Dawley rats, intact or surgically gonadectomized (Gx), received testosterone (T) or 17β-estradiol (E2) via subdermal SILASTIC (Dow Corning Corp.) implants; a subset of male rats received dihydrotestosterone. After 21 days, animals were anesthetized, and hearts were excised and subjected to ex vivo regional ischemia-reperfusion (I-R). Hearts from intact males had larger infarcts than those from females following I-R; Gx produced the opposite effect, confirming a role for sex steroids. In Gx males, androgens (dihydrotestosterone, T) and E2 aggravated I-R-induced cardiac damage, whereas in Gx females, T had no effect and E2 reduced infarct area. Increased circulating T levels up-regulated androgen receptor and receptor for advanced glycation end products, which resulted in enhanced apoptosis aggravating cardiac damage in both males and females. In conclusion, our study demonstrates, for the first time, that sex steroids regulate autophagy during myocardial infarction and shows that a novel mechanism of action for androgens during I-R is down-regulation of antiapoptotic protein Bcl-xL (B cell lymphoma-extra large), a key controller for cross talk between autophagy and apoptosis, shifting the balance toward apoptosis and leading to aggravated cardiac damage.

A sequential interferon gamma directed chemotactic cellular immune response determines survival and cardiac function post-myocardial infarction

2019 ◽  
Vol 115 (13) ◽  
pp. 1907-1917 ◽  
Author(s):  
Stefanie Finger ◽  
Maike Knorr ◽  
Michael Molitor ◽  
Rebecca Schüler ◽  
Venkata Garlapati ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Immune Response ◽  
Inflammatory Response ◽  
Cardiac Function ◽  
Interferon Gamma ◽  
Cellular Immune Response ◽  
Post Myocardial Infarction ◽  
Ifn Γ ◽  
Cellular Immune

Abstract Aims Myelomonocytic cells are critical in injury and healing post-myocardial infarction (MI). Mechanisms of regulation, however, are incompletely understood. The aim of the study was to elucidate the role of interferon gamma (IFN-γ) in the orchestrated inflammatory response in a murine model of MI. Methods and results MI was induced in 8- to 12-week-old male mice (C57BL/6 background) by permanent ligation of the left anterior descending (LAD) coronary artery. Lysozyme M (LysM)+ cell-depleted LysMiDTR transgenic mice displayed a reduced influx of CD45.2+/CD3−/CD11b+/Gr-1high neutrophils into infarcted myocardium 1 day post-MI compared with infarcted controls, paralleled by decreased cardiac mRNA levels of IFN-γ and tumour necrosis factor alpha (TNF-α). Mortality after MI was significantly increased in LysM+ cell-depleted mice within 28 days post-MI. To more specifically address the role of neutrophils, we depleted C57BL/6 mice with a monoclonal anti-Gr-1 antibody and found increased mortality, deteriorated cardiac function as well as decreased cardiac IFN-γ mRNA expression early after MI. Ccl2, Cxcl1, Cx3cl1, and Il12b mRNA were reduced 3 days after MI, as was the amount of CD11b+/Ly-6G−/Ly-6Chigh inflammatory monocytes. LAD-ligated Cramp−/− mice lacking cathelicidin important in neutrophil-dependent monocyte chemotaxis as well as IFNγ−/− and TNFα−/− mice phenocopied Gr-1+ cell-depleted mice, supporting a regulatory role of IFN-γ impacting on both the sequence of inflammatory cell invasion and cardiac outcome early after MI. The use of conditional IFN-γ receptor deficient mice indicated a direct effect of IFN-γ on LysM+ cells in cardiac injury post-MI. Using IFN-γ reporter mice and flow cytometry, we identified cardiac lymphoid cells (CD4+ and CD8+ T cells and natural killer cells) as primary source of this cytokine in the cardiac inflammatory response post-MI. Conclusion IFN-γ directs a sequential chemotactic cellular immune response and determines survival and cardiac function post-MI.

scholarly journals Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Annie Turkieh ◽  
Henri Charrier ◽  
Emilie Dubois-Deruy ◽  
Sina Porouchani ◽  
Marion Bouvet ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Noncoding Rnas ◽  
Cell Types ◽  
Cardiac Cells ◽  
Left Ventricle Remodeling ◽  
Pathological Conditions ◽  
Evolutionarily Conserved ◽  
Different Cell Types

Macroautophagy is an evolutionarily conserved process of the lysosome-dependent degradation of damaged proteins and organelles and plays an important role in cellular homeostasis. Macroautophagy is upregulated after myocardial infarction (MI) and seems to be detrimental during reperfusion and protective during left ventricle remodeling. Identifying new regulators of cardiac autophagy may help to maintain the activity of this process and protect the heart from MI effects. Recently, it was shown that noncoding RNAs (microRNAs and long noncoding RNAs) are involved in autophagy regulation in different cell types including cardiac cells. In this review, we summarized the role of macroautophagy in the heart following MI and we focused on the noncoding RNAs and their targeted genes reported to regulate autophagy in the heart under these pathological conditions.

scholarly journals Targeting Inflammation after Myocardial Infarction: A Therapeutic Opportunity for Extracellular Vesicles?

2021 ◽  
Vol 22 (15) ◽  
pp. 7831
Author(s):  
Margarida Viola ◽  
Saskia C. A. de Jager ◽  
Joost P. G. Sluijter
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Extracellular Vesicles ◽  
Cardiac Inflammation ◽  
Stem And Progenitor Cells ◽  
Therapeutic Opportunity ◽  
Strong Inflammatory Response ◽  
Non Coding Rnas ◽  
Dead Tissue

After myocardial infarction (MI), a strong inflammatory response takes place in the heart to remove the dead tissue resulting from ischemic injury. A growing body of evidence suggests that timely resolution of this inflammatory process may aid in the prevention of adverse cardiac remodeling and heart failure post-MI. The present challenge is to find a way to stimulate this process without interfering with the reparative role of the immune system. Extracellular vesicles (EVs) are natural membrane particles that are released by cells and carry different macromolecules, including proteins and non-coding RNAs. In recent years, EVs derived from various stem and progenitor cells have been demonstrated to possess regenerative properties. They can provide cardioprotection via several mechanisms of action, including immunomodulation. In this review, we summarize the role of the innate immune system in post-MI healing. We then discuss the mechanisms by which EVs modulate cardiac inflammation in preclinical models of myocardial injury through regulation of monocyte influx and macrophage function. Finally, we provide suggestions for further optimization of EV-based therapy to improve its potential for the treatment of MI.

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