Myocardial infarction induces early increased remote ADAM8 expression of rat hearts after cardiac arrest

Vuohelainen, Vilma; Raitoharju, Emma; Levula, Mari; Lehtimäki, Terho; Pelto‐Huikko, Markku; Honkanen, Teemu; Huovila, Ari; Paavonen, Timo; Tarkka, Matti; Mennander, Ari

doi:10.3109/00365513.2011.591424

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…The association of this inflammatory change with myocardial tissue damage after heterotopic heart transplantation is already well observed in many previous studies. [28]…”

Section: Discussionmentioning

confidence: 99%

Oxytocin ameliorates the immediate myocardial injury in heart transplant through down regulation of the neutrophil dependent myocardial apoptosis

Al-Amran

Shahkolahi

2014

Heart Views

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Cardiac oxytocin (OT) is structurally identical to that found in the hypothalamus, which thereby indicates that cardiac OT is derived from the same gene and is an active form of OT. The abundance of OT and OT receptors in atrial myocytes shows that, directly and/or via the release of the cardiac hormone atrial natriuretic peptide, OT can regulate the force of cardiac contractions. Previous studies have demonstrated the role of OT in the myocardial inflammatory response. The mechanism by which OT elicits protective myocardial effects in the immediate post-transplantation period is not yet clear, and the role of the early phase inflammatory elements in this mechanism has not yet been studied. As a result, in this study, we have investigated the anti-inflammatory effects of OT on myocardial protection in the immediate post-transplantation period.Methods:Adult male Albino rats were grouped into: Sham, Control, and OT-treated groups. The control and treated groups sustained cervical heterotopic heart transplant. Myocardial injury was assessed by measuring: Plasma cardiac troponin I, myocardial proinflammatory cytokines, and histopathological assessment for score of injury, and degree of apoptosis. Myocardial myeloperoxidase, neutrophil infiltration, and neutrophil chemotactant agents, reactive oxygen species, and reactive nitrogen species formation all were measured in the myocardium after 3 hour of reperfusion to assess the neutrophil-dependant myocardial injury and the mechanism involved.Results:Oxytocin down-regulates the neutrophil chemotactant agents the KC/CXCL1 and MIP-2/CXCL2 which recruit less neutrophil into myocardium, this decrement in myocardial PMN infiltration is associated with less reactive oxygen species and reactive nitrogen species formation in the myocardium after 3 hours of global ischemia reperfusion. These oxytocin-induced down-regulation inflammatory and oxidative processes will end in less myocardial injury through impedance in the post-myocardial ischemia/reperfusion apoptotic process.Conclusion:Oxytocin ameliorates myocardial injury in heart transplant through down-regulation the myocardial inflammatory response, reactive oxygen species, and neutrophil-dependant myocardial apoptosis.

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“…The association of this inflammatory change with myocardial tissue damage after heterotopic heart transplantation is already well observed in many previous studies. [28]…”

Section: Discussionmentioning

confidence: 99%

Oxytocin ameliorates the immediate myocardial injury in heart transplant through down regulation of the neutrophil dependent myocardial apoptosis

Al-Amran

Shahkolahi

2014

Heart Views

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“…A modified heterotopic transplantation of the heart was performed to all 16 grafts, as previously described [4]. Briefly, before harvesting, cold 4 o C infusion with cardioplegia fluid (Custodiol ® ; Bretschneider HTK solution for cardioplegia and miltiorgan protection, Germany) was infused into the donor aorta in order to arrest the heart and maximize myocardial protection.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…This animal model mimics the clinical concept of having an area of local and persisting MI after complete revascularization of the globally ischemic heart. Using this experimental model, we have recently demonstrated that MI after IRI has a remote myocardial impact after cardiac arrest [4].…”

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confidence: 99%

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C4d Deposition Reveals Myocardial Infarction After Cardiac Arrest -Experimental Study

Vuohelainen¹,

Paavonen²,

Hämäläinen³

et al. 2015

Adv Clin Exp Med

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Background. The diagnosis of regional myocardial infarction (MI) after cardiac arrest and ischemia-reperfusion injury (IRI) is a major clinical challenge. Objectives. We evaluated in a rat cardiac transplantation model whether IRI alone or with MI would induce complement C4d deposition. Material and Methods. Isogenic heterotopic cardiac transplantation was performed in 16 Fischer 344 rats to induce IRI, of which 9 rats also underwent ligation of the left anterior coronary artery (LAD) of the heart to yield MI. Histology and qRT-PCR for endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS) and transforming growth factor β (TGFβ) were performed after cessation of heart beat. C4d was evaluated by immunohistochemistry. Results. Myocardial inflammation and C4d deposition was increased in grafts with IRI+MI as compared with IRI (0.71 vs. 0.14, PSU, respectively, p < 0.04 and 80.13 vs. 20.29, PSU, respectively, p < 0.02). The expression of eNOS decreased in grafts with IRI + MI as compared with IRI (p < 0.05). Receiver operating characteristic (ROC) curve analysis showed that IRI + MI was associated with C4d deposition (AUC 0.837; S.E. 0.116; p = 0.035; 95% C.I. 0.610-1.000). Conclusions. Increased C4d deposition may be amenable to identify early MI after cardiac arrest. Early treatment aimed towards complement activation may provide a novel means for induced MI after cardiac arrest (Adv Clin Exp Med 2015, 24, 3, 393-399).

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“…Most members of ADAM families had been recognized to function in a range of biological processes, including myoblast differentiation and growth factor secretion 7, 8. Later on, several studies revealed that ADAM family also participated in cardiovascular development9, 10, 11, 12, 13 or cardiomyopathies 9, 14, 15, 16. Notably, a previous investigation suggested that ADAM10/12/15/17 expressions were increasing in both human dilated cardiomyopathy and (or) hypertrophic obstructive cardiomyopathy 17.…”

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confidence: 99%

ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK‐AKT Signaling

Xiang

Luo

et al. 2018

JAHA

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BackgroundCardiac hypertrophy has been recognized as an important independent risk factor for the development of heart failure and increases the risk of cardiac morbidity and mortality. A disintegrin and metalloprotease 23 (ADAM23), a member of ADAM family, is involved in cancer and neuronal differentiation. Although ADAM23 is expressed in the heart, the role of ADAM23 in the heart and in cardiac diseases remains unknown.Methods and ResultsWe observed that ADAM23 expression is decreased in both failing human hearts and hypertrophic mice hearts. Cardiac‐specific conditional ADAM23‐knockout mice significantly exhibited exacerbated cardiac hypertrophy, fibrosis, and dysfunction, whereas transgenic mice overexpressing ADAM23 in the heart exhibited reduced cardiac hypertrophy in response to pressure overload. Consistent results were also observed in angiotensin II‐induced neonatal rat cardiomyocyte hypertrophy. Mechanistically, ADAM23 exerts anti‐hypertrophic effects by specifically targeting the focal adhesion kinase‐protein kinase B (FAK‐AKT) signaling cascade. Focal adhesion kinase inactivation by inhibitor (PF‐562271) greatly reversed the detrimental effects in ADAM23‐knockout mice subjected to aortic banding.ConclusionAltogether, we identified ADAM23 as a negative regulator of cardiac hypertrophy through inhibiting focal adhesion kinase‐protein kinase B signaling pathway, which could be a promising therapeutic target for this malady.

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Myocardial infarction induces early increased remote ADAM8 expression of rat hearts after cardiac arrest

Abstract: Remote histopathological changes of ischemic cardiac grafts are associated with increased expression of ADAM8 thus emphasizing a global myocardial impact of MI.

Cited by 18 publications

References 30 publications

Oxytocin ameliorates the immediate myocardial injury in heart transplant through down regulation of the neutrophil dependent myocardial apoptosis

Oxytocin ameliorates the immediate myocardial injury in heart transplant through down regulation of the neutrophil dependent myocardial apoptosis

C4d Deposition Reveals Myocardial Infarction After Cardiac Arrest -Experimental Study

ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK‐AKT Signaling

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