E-selectin gene haplotypes are associated with the risk of myocardial infarction

Gorący, Jarosław; Kaczmarczyk, Mariusz; Ciechanowicz, Andrzej; Safranow, Krzysztof; Goracy, J; Jakubowska, Katarzyna; Chlubek, Dariusz; Gorący, Iwona

doi:10.5114/aoms.2019.84413

Cited by 5 publications

(4 citation statements)

References 35 publications

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“…Oxidative stress reduction has been reported to prevent injury of myocardial tissues [21], and the results of our study also show that treatment with mRNA-103 inhibitor reduces the increased level of oxidative stress. Myocardial infarction occurs due to hypoxia to the myocardial tissues, which activates the apoptosis pathway and increases the apoptosis of myocardiocytes [22][23][24][25]. Apoptosis of myocardiocytes contributes to the degeneration of myocardial tissues, which leads to MI.…”

Section: Discussionmentioning

confidence: 99%

mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway

Fan

Liu

et al. 2020

Arch Med Sci

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Introduction: This investigation determined the cardioprotective activity of mRNA-103 inhibitor against myocardial infarction (MI) and also evaluated its molecular mechanism. Material and methods: MI was induced in rats by inducing myocardial ischaemia/reperfusion (I/R), and left ventricular (LV) mRNA-103 (1 × 10 7 TU) was injected into the myocardium around the infarcted area. The effect of mRNA-103 inhibitor was assessed by determining the levels of myocardial enzymes and cytokines in the serum, the myeloperoxidase (MPO) activity, and the levels of Toll-like receptor 4 (TLR4), nuclear factor k-light-chain enhancer of activated B cells (NF-kB), and MyD88 mRNAs in the myocardial tissues of MI rats. Immunocytochemical analysis and a histopathology study were also performed. Results: The levels of myocardial enzymes and cytokines were lower in the mRNA-103 inhibitor-treated group than in the group in which the only treatment was the induction of MI. There was a lower percentage of infarcted area and a lower apoptosis index in the mRNA-103 inhibitor-treated group compared to the MI-only. The levels of TLR4, NF-kB, and MyD88 mRNAs were lower in the myocardial tissues of the mRNA-103 inhibitor-treated group than in the MI-only group. Immunohistochemical analysis revealed that treatment with mRNA-103 inhibitor ameliorated the expression of TLR4 in the myocardial tissues of MI rats. Conclusions: The data revealed that inhibition by mRNA-103 protects against myocardial injury in MI rats by regulating the inflammasome pathway.

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Section: Discussionmentioning

confidence: 99%

mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway

Fan

Liu

et al. 2020

Arch Med Sci

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“…Myocardial infarction is myocardial necrosis caused by the interruption of coronary blood flow [ 13 , 14 ]. Partial cardiomyocyte necrosis occurs due to severe and persistent ischemia [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of ivabradine on ventricular electrophysiological remodeling after myocardial infarction in rats

et al. 2020

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IntroductionThis study aims to investigate the effects of ivabradine (IVA) on ventricular electrophysiological remodeling after myocardial infarction (MI) in rats.Material and methodsA total of 60 male Sprague-Dawley rats were randomly divided into five groups: an MI group, an IVA group, a metoprolol (MET) group, an IVA + MET group, and a sham group. After a four-week intervention, the ventricular electrophysiological parameters were detected by multichannel electrophysiological polygraph. Then, the morphological characteristics were evaluated using hematoxylin and eosin (H&E) and Masson’s staining, and the expression of phosphorylated connexin 43 (p-Cx43) in the left ventricular wall was detected through immunohistochemistry and the Western blot test.ResultsThe electrophysiological examination revealed that the induction rate and fatality rate of ventricular tachycardia (VT)/ventricular fibrillation (VF) were lower in both the IVA and the MET group, compared with the MI group (6/12, 6/12 vs. 10/11; and 1/12, 1/12 vs. 5/11; all p < 0.05), as well as the IVA + MET group (1/11 vs. 10/11, p < 0.01; and 1/11 vs. 5/11, p < 0.05). The induction rate of VT/VF was lower in the IVA + MET group, compared to the MET group (1/11 vs. 6/12, p < 0.05). H&E and Masson’s staining revealed that compared with the MI group, the left ventricular infarction area was lower in the IVA, MET, and IVA + MET groups (p < 0.05, p < 0.05, and p < 0.01, respectively), while collagen volume fraction (CVF) also was lower in the other groups (all p < 0.01). The left ventricular infarction area and CVF both were lower in the IVA + MET group, compared to the MET group (p < 0.05 and p < 0.01, respectively). The immunohistochemistry and Western blot revealed that p-Cx43 expression was higher in the treatment groups, compared with the MI group (all p < 0.01).ConclusionsIVA can reduce the incidence of ventricular arrhythmia after MI in male rats by improving both structural and electrical remodeling, and the combination of IVA and MET is even more effective.

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“…Наиболее изученным полиморфизмом SELE в отношении риска ИБС является 128Arg. В частности, с риском развития ИМ были связаны rs5361 (561 A/С) и G98T (rs1805193) [24,25]. Влияние генотипа C/C rs5353 на риск развития ИМ в нашей работе показано впервые.…”

Section: результатыunclassified

Gene polymorphism and serum levels of some angiogenic growth factors and pro- and anti-inflammatory cytokines in patients with post-infarction cardiac remodeling

Nikolaeva,

Babushkina,

Ryabova

et al. 2024

Russ J Cardiol

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Aim. To investigate the polymorphic variants of IL10, FGF2, VEGFD, TRAIL, SELE, TNFA and TNFβ genes in patients with primary ST-segment elevation myocardial infarction (MI) (STEMI) and to evaluate their association with late post-infarction cardiac remodeling.Material and methods. The study includes 74 patients age 61±10,7 years with primary STEMI. Percutaneous coronary intervention with restoration of infarct-related artery patency was performed in all patients after 60 (40; 80) minutes since admission to the hospital. Serum levels of fibroblast growth factor (FGF), interleukin-10 (IL-10), tumor necrosis factor family cytokines (TNF-α, TNF-β and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)) were measured with the Multiplex Instrument FLEXMAP 3D system (Luminex Corporation) and the MILLIPLEX Human Cytokine/Chemokine Panel II on the 1st, 7th day of early post-MI period and after 6 and 12 months. The late adverse cardiac remodeling was determined after 12 months of long-term post-MI period according to 2D echocardiography. The increase in left ventricular end-diastolic volume by 15% or more by 12 months was considered late adverse cardiac remodeling. The patients were genotyped by 16 single-nucleotide polymorphisms (SNPs) in the TNFβ, TNF, Il10, TNFRSF1B, VEGFD, TRAIL, FGF2, SELE genes.Results. Adverse cardiac remodeling occurred in 19 patients (25,7%). The genetic association analysis revealed the significant association of rs1800629 TNFA (χ2=4,748; p=0,029), rs5353 SELE (χ2=10,85; p=0,004) and rs6632528 VEGFD (χ2=8,127; p=0,017) with an increased risk of STEMI. Higher concentration of IL-10 was detected on the 7th day of MI (p=0,05) and 6 months later (p=0,028) in A/T rs3024492 genotype carriers, as well as FGF in T/T rs13122694 genotype carriers by the 6th month after the event (p=0,04). The dependence of the main LV indicators on the distribution of polymorphism genotypes rs3024492 IL10, rs13122694 FGF2 and rs4830939 VGEFD was discovered. In the first 24 hours of MI in rs3024492 IL10 heterozygotes, LV contractile function was worse in comparison with T/T genotype carriers. Also, carriers of the T/T rs13122694 FGF2 genotype were distinguished by higher LV ejection fraction, longitudinal global LV deformation and lower of LV end-systolic index in the early post-infarction period. In the long-term post-infarction period, T/T rs4830939 VEGFD carriers differed in a greater LV dilation than carriers of the C/C and C/T genotypes.Conclusion. The study showed the contribution of polymorphism of the inflammation system genes to a predisposition to STEMI — both at the levels of phenotype and individual signs.

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E-selectin gene haplotypes are associated with the risk of myocardial infarction

Cited by 5 publications

References 35 publications

mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway

mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway

Effects of ivabradine on ventricular electrophysiological remodeling after myocardial infarction in rats

Gene polymorphism and serum levels of some angiogenic growth factors and pro- and anti-inflammatory cytokines in patients with post-infarction cardiac remodeling

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