Coronary sinus concentrations of interleukin 6 and its soluble receptors are affected by reperfusion and may portend complications in patients with myocardial infarction

Kamiński, Karol; Kożuch, Marcin; Bonda, Tomasz A.; Wojtkowska, Izabela; Kozieradzka, Anna; Dobrzycki, Sławomir; Kralisz, Paweł; Nowak, Konrad; Prokopczuk, Przemysław; Winnicka, Maria M.; Musiał, Włodzimierz J.

doi:10.1016/j.atherosclerosis.2009.03.033

Cited by 29 publications

(19 citation statements)

References 23 publications

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“…myocardial infarction and its complications [12], congestive heart failure, hypertrophic cardiomyopathy, but the prevalence of sIL-6R and sgp130 and its potential role in PAH have never been studied. As IL-6 mediated effect depends on its interplay with the receptors, we hypothesize that increased concentrations of soluble IL-6R in PAH could be important for the systemic amplification of IL-6 signaling in a variety of tissues.…”

Section: Introductionmentioning

confidence: 98%

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

et al. 2015

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Section: Introductionmentioning

confidence: 98%

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

et al. 2015

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“…Glomerular filtration rate declines early following myocardial infarction and persists as a chronic abnormality and is accompanied by initial transient macrophage infiltration and progressive fibrosis of the renal interstitium. Upregulation of proinflammatory interleukin 6 (IL-6) after myocardial infarction [3,4], in addition to the induction of other proinflammatory cytokines, compromises cardiac performance, and is postulated to be one of early predictive factors for secondary acute kidney injury [5]. In chronic heart failure (CHF), level of IL-6 is elevated proportionally to the severity of circulatory insufficiency [6], and is an independent predictor of mortality [7].…”

Section: Introductionmentioning

confidence: 99%

CCN1 expression in interleukin-6 deficient mouse kidney in experimental model of heart failure

Bonda

Taranta

Kamiński

et al. 2013

Folia Histochem Cytobiol.

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Chronic heart failure often leads to worsening of the renal function. Mediators of this process include inflammatory and neuroendocrine factors. CCN1 (Cyr 61), a member of growth factor-inducible immediate early genes, which modulates inflammation and fibrogenesis, is excreted with urine in the early phase of acute renal injury and may be involved in the pathogenesis of the cardiorenal syndrome. The aim of the study was to evaluate CCN1 protein abundance and localization in the kidney of IL-6-deficient C57BL/6J (IL-6 KO) mice and respective wild-type (WT) animals in basal conditions and in animals with chronic heart failure twelve weeks after myocardial infarction. Age-and sex-matched mice from both strains subjected to sham operation served as controls. One group of WT animals subjected to myocardial infarction was treated with antagonist of AT1 receptor telmisartan over 12 weeks. Abundance and localization of CCN1 protein in kidney were assessed with Western blotting and immunohistochemistry, respectively. In all groups the strongest immunohistochemical reaction for CCN1 was observed in distal convoluted tubules and in smaller arteries, however, the total expression of CCN1 protein was lower in IL-6 KO mice in comparison to WT animals. The main difference in CCN1 distribution between the examined genotypes was lack of reaction in internal renal medulla and very weak reaction in proximal convoluted tubules in IL-6 KO mice. Experimental heart failure only slightly attenuated the expression of CCN1 protein in the kidney of WT mice and had no effect in IL-6 KO mice. Although, blockade of AT1 receptor did not alter CCN1 protein expression in kidneys of WT mice after myocardial infarction, it significantly changed its CCN1 distribution in the renal tubular system. (Folia Histochemica et Cytobiologica 2013, Vol. 51, No. 1, 84-91)

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“…Mitochondrial dysfunction promotes the cellular irreversible damage (21)(22)(23). The inflammatory response leads to microcirculation dysfunction (41)(42)(43) and tissue damage (44)(45)(46)(47). However, the relationship between the inflammatory response and mitochondrial dysfunction in the IRI process has not been revealed.…”

Section: Discussionmentioning

confidence: 98%

Glycogen Synthase Kinase 3β Inhibition Protects the Cardiomyocytes from Anoxia/Reoxygenation Injury by Modulating Inﬂammatory Response and Reducing the Opening of mPTP

Cheng¹,

Jun²,

Xue³

et al. 2015

J Anesth Perioper Med

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Background: Phosphorylation of glycogen synthase kinase 3β (GSK-3β) is crucial in multiple cardioprotective signaling pathways. But the downstream mechanism is unclear. Considering GSK-3β is the key regulator of nuclear factor-κB (NF-κB) and mitochondrial permeability transition pore (mPTP) is a critical determinant of lethal reperfusion injury, we assessed the mechanism of postconditioning with the selective inhibitor of GSK-3β associated with modulating in fl ammatory response and reducing the opening of mPTP. Methods: After cultured for 72 hours, neonatal rat cardiomyocytes were randomly divided into 3 groups according to random number table: Sham group, anoxia/reoxygenation injury group (AR group) and GSK-3β inhibitor TDZD -8 postconditioning group (TDZD -8 group). At the end of the experiment, the lactate dehydrogenase (LDH) release rate, myocardial apoptosis and the supernatant concentrations of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were measured. The NF-κBp65 and phosphorylated NF-κBp65Ser536 in all samples were assessed by western-blotting technique. The mitochondrial membrane potential was measured by rhodamine 123 staining flow cytometry and confocal laser scanning microscope. Results: We discovered that postconditioning with GSK-3β inhibitor TDZD -8 could significantly protect against cardiomyocyte anoxia/reoxygenation injury, as shown by reducing the early apoptosis and LDH release rate. And this cardioprotective method could significantly attenuate inflammatory response to the anoxia/reoxygenation injury, as evidenced by decreasing the activity of NF-κB and levels of inflammatory cytokines, such as IL-6 and TNF-α. Furthermore, it could significantly reduce the irreversibly high level opening of the mPTP, as evidenced by increasing the mitochondrial membrane potential of anoxia/reoxygenation cardiomyocyte. Conclusions: Our current results indicated that postconditioning with GSK-3β inhibitor TDZD -8 significantly attenuated the systemic inflammatory and reduced the opening of mPTP response to cardiomyocytes anoxia/reoxygenation injury.

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Coronary sinus concentrations of interleukin 6 and its soluble receptors are affected by reperfusion and may portend complications in patients with myocardial infarction

Cited by 29 publications

References 23 publications

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

CCN1 expression in interleukin-6 deficient mouse kidney in experimental model of heart failure

Glycogen Synthase Kinase 3β Inhibition Protects the Cardiomyocytes from Anoxia/Reoxygenation Injury by Modulating Inﬂammatory Response and Reducing the Opening of mPTP

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