Short-term exercise training improves cardiac function associated to a better antioxidant response and lower type 3 iodothyronine deiodinase activity after myocardial infarction

Abstract Aims Neutrophils have both detrimental and beneficial effects in myocardial infarction (MI), but little is known about the underlying pathways. S100A8/A9 is a pro-inflammatory alarmin abundantly expressed in neutrophils that is rapidly released in the myocardium and circulation after myocardial ischaemia. We investigated the role of S100A8/A9 in the innate immune response to MI. Methods and results In 524 patients with acute coronary syndrome (ACS), we found that high plasma S100A8/A9 at the time of the acute event was associated with lower left ventricular ejection fraction (EF) at 1-year and increased hospitalization for heart failure (HF) during follow-up. In wild-type C57BL/6 mice with MI induced by permanent coronary artery ligation, treatment with the S100A9 blocker ABR-238901 during the inflammatory phase of the immune response inhibited haematopoietic stem cell proliferation and myeloid cell egression from the bone marrow. The treatment reduced the numbers of neutrophils and monocytes/macrophages in the myocardium, promoted an anti-inflammatory environment, and significantly improved cardiac function compared with MI controls. To mimic the clinical scenario, we further confirmed the effects of the treatment in a mouse model of ischaemia/reperfusion. Compared with untreated mice, 3-day ABR-238901 treatment significantly improved left ventricular EF (48% vs. 35%, P = 0.002) and cardiac output (15.7 vs. 11.1 mL/min, P = 0.002) by Day 21 post-MI. Conclusion Short-term S100A9 blockade inhibits inflammation and improves cardiac function in murine models of MI. As an excessive S100A8/A9 release is linked to incident HF, S100A9 blockade might represent a feasible strategy to improve prognosis in ACS patients.

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Effect of low grade exercise training and a vasodilator on cardiac function in patients with recent myocardial infarction.

Japanese Circulation Journal ◽

10.1253/jcj.54.11_1426 ◽

1990 ◽

Vol 54 (11) ◽

pp. 1426-1429 ◽

Cited By ~ 2

Author(s):

MITSUHIRO YOKOTA ◽

JITSUKI TSUZUKI ◽

HARUO INAGAKI ◽

MAKOTO WATANABE ◽

TATSUYUKI MATSUNAMI ◽

...

Keyword(s):

Myocardial Infarction ◽

Exercise Training ◽

Cardiac Function ◽

Low Grade ◽

Recent Myocardial Infarction

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Short-term exercise training effect after myocardial infarction on myocardial oxygen consumption indices and ischemic threshold

Archives of Physical Medicine and Rehabilitation ◽

10.1016/s0003-9993(95)80613-x ◽

1995 ◽

Vol 76 (3) ◽

pp. 262-265 ◽

Cited By ~ 10

Author(s):

Athanasios Tsoukas ◽

Haritos Andonakoudis ◽

Stamatios Christakos

Keyword(s):

Myocardial Infarction ◽

Oxygen Consumption ◽

Exercise Training ◽

Myocardial Oxygen Consumption ◽

Training Effect ◽

Short Term

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PL - 027 Up-regulation of NRG1 improves cardiac repair in zebra fish and involved in the cardioprotective effects of exercise training in rats of myocardial infarction

Exercise Biochemistry Review ◽

10.14428/ebr.v1i1.8453 ◽

2018 ◽

Vol 1 (1) ◽

Author(s):

Mengxin Cai ◽

Shaojun Du ◽

Zhenjun Tian

Keyword(s):

Myocardial Infarction ◽

Skeletal Muscle ◽

Exercise Training ◽

Cardiac Function ◽

Signaling Pathway ◽

Heart Development ◽

Cardiac Repair ◽

Cardiomyocyte Proliferation ◽

Infarcted Heart ◽

Cardioprotective Effects

Objective Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Exercise training could improve cardiac function following MI. However, the mechanisms are still not well-known. Neuregulin 1 (NRG1)plays an important role in heart development and regeneration.In this study, we investigated the effect of NRG1 on cardiac regeneration in a zebrafish model, detected whether exercise could improve cardiac function through regulating NRG1 expression in infarcted heart and explore the possible role of up-regulation of NRG1 in skeletal muscle play in the cardioprotective effects in rats with MI. Methods Transgenic zebrafish line, cmlc2:CreERandβ-act2:BSNrg1,wereusedto study the effect of NRG1 on heart growth and regeneration after injury. PCNA was detected by immunofluorescence staining andmRNAexpression of gata4, nkx2.5, tbx5, smyd1b, hsp90α and murf were tested by RT-PCR.Sprague-Dawley rats were used to establish MI model and underwent fourweeks of exercise training (ET) or pAAV-{dMCK promoter}rNRG1-eGFP intervention.AG1478 was used asan inhibitor of NRG1/ErbBs signaling pathway. Cardiac function and structure,cardiomyocyte proliferation and NRG1 expression were detected in the heart or skeletal. Results Cardiac-specific overexpression of NRG1 induced cardiac hypertrophy and cardiomyocyte proliferation, regulated the mRNA expression of gata4, nkx2.5, tbx5, smyd1b, hsp90α andmurf in uninjuriedzebrafish, and promote cardiac repair and regeneration after injury in the zebrafish.Exercise activated NRG1/ErbBs signaling pathway, improved cardiac remodeling and heart function, enhanced cardiomyocyte proliferation, reduced cardiomyocyte apoptosis, ROS level and MuRF1 protein expression in rats with MI. BlockingErbB signaling attenuated the ET-induced cardioprotection effects in rat with MI.up-regulation of NRG1 expression in skeletal muscle could increase the protein level of NRG1 in serum and infarcted heart, improve cardiomyocyte proliferation and reduce the level of cardiac fibrosis, finally promote cardiac function. Conclusions Up-regulation of NRG1 expression in the heart or skeletal musclemay be one of the underlying mechanisms of thebeneficial effects of exercise training following MI.

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Statin Administration Does Not Improve the Mobilization of Very Small Embryonic-Like Stem Cells (VSELs) in Contrast to Resveratrol Treatment in a Murine Model of Acute Myocardial Infarction

Physiological Research ◽

10.33549/physiolres.932390 ◽

2012 ◽

pp. 543-549 ◽

Cited By ~ 6

Author(s):

H. WANG ◽

Y.-J. YANG ◽

H.-Y. QIAN ◽

Q. ZHANG ◽

L.-J. GAO ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Stem Cell ◽

Cardiac Function ◽

Stromal Cell ◽

Statin Treatment ◽

Positive Control ◽

Short Term ◽

Cellular Cardiomyoplasty ◽

Stromal Cell Derived Factor

We have found that short-term statin treatment plus stem cell transplantation in acutely infarcted hearts improves cardiac function because statins promote the efficacy of cellular cardiomyoplasty. Autologous Sca-1+Lin-CD45-(CXCR+) very small embryonic-like stem cell (VSEL) mobilization in acute myocardial infarction (AMI) correlates with the preservation of cardiac function. Whether short-term atorvastatin (Ator) can enhance the mobilization or recruitment of VSELs in AMI is still unclear. We divided mice into 4 groups: 1) sham; 2) AMI; 3) AMI+resveratrol (RSV) as a positive control; and 4) AMI+Ator. There was an increase in the circulating VSEL/full population of leukocytes (FPL) ratio 48 hours after AMI, and AMI+RSV increased it further. Ator administration did not increase the VSEL/FPL ratio. The cardiac stromal cell-derived factor-1 (SDF-1) and SDF-1α levels were in agreement with the results of VSEL mobilization. One week after AMI, more Sca-1+CXCR+ cells were recruited to the myocardium of AMI+RSV mice but not AMI+Ator mice. Short-term Ator administration failed to upregulate cardiac SDF-1 and could not enhance the recruitment of VSELs early after AMI.

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