L-type Ca2+ channels’ involvement in IFN-γ-induced signaling in rat ventricular cardiomyocytes

Mitrokhin, Vadim; Филатова, Т. С.; Shim, Andrey; Bilichenko, A. S.; Abramochkin, Denis V.; Kamkin, Andre; Mladenov, Mitko

doi:10.1007/s13105-019-00662-y

Cited by 8 publications

(5 citation statements)

References 26 publications

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“…The maximum peak current was observed at 0 mV and in ventricular cells it was significantly greater than in atrial myocytes. It is noteworthy that the peak amplitude of I Ca in ventricular cells was remarkably high (−10.2±1.15 pA pF −1 ) in comparison with I Ca recorded in mammalian cardiomyocytes in similar conditions (Mitrokhin et al, 2019;Ogura et al, 1999) indicating robust trans-sarcolemmal influx in the ventricular cells. In line with findings in embryonic chicken myocytes (Kitchens et al, 2003), we found that 50 μmol l −1 nifedipine completely abolished I Ca in both atrial and ventricular cells from quail (not shown).…”

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confidence: 68%

Warmer, faster, stronger: Ca2+ cycling in avian myocardium

Филатова

Abramochkin

Shiels

2020

Journal of Experimental Biology

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Birds occupy a unique position in the evolution of cardiac design. Their hearts are capable of cardiac performance on par with, or exceeding that of mammals, and yet the structure of their cardiomyocytes resemble those of reptiles. It has been suggested that birds use intracellular Ca2+ stored within the sarcoplasmic reticulum (SR) to power contractile function but neither SR Ca2+ content nor the cross-talk between channels underlying Ca2+-induced Ca2+-release (CICR) have been studied in adult birds. Here we used voltage clamp to investigate the Ca2+ storage and refilling capacities of the SR and the degree of transsarcolemmal and intracellular Ca2+ channel interplay in freshly isolated atrial and ventricular myocytes from the heart of the Japanese quail (Coturnix japonica). A transsarcolemmal Ca2+ current was detectable both in quail atrial and ventricular myocytes and was mediated only by L-type Ca2+ channels. The peak density of ICa was larger in ventricular cells than in atrial and exceeded that reported for mammalian myocardium recorded under similar conditions. Steady-state SR Ca2+ content of quail myocardium was also larger than that reported for mammals and reached 750.6±128.2 µmol l−1 in atrial cells and 423.3±47.2 µmol l−1 in ventricular cells at 24⁰C. We observed SR-Ca2+-dependent inactivation of ICa in ventricular myocytes indicating cross-talk between sarcolemmal Ca2+ channels and ryanodine receptors in the SR. However, this phenomenon was not observed in atrial myocytes. Taken together, these findings help to explain the high efficiency avian myocyte excitation-contraction coupling with regard to their reptilian-like cellular ultrastructure.

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confidence: 68%

Warmer, faster, stronger: Ca2+ cycling in avian myocardium

Филатова

Abramochkin

Shiels

2020

Journal of Experimental Biology

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“…Inflammatory cytokines, such as TNFa, IL1b and IL17, can significantly enhance the risk of arrhythmic events by directly promoting electrical and structural cardiac remodeling 45 . In addition, IFNg has been shown to exert a sustained inhibitory effect on cardiac L-type calcium channels 60 and to induce a metabolic shift in cardiomyocytes with downregulation of OXPHOS, which is consistent with the failing heart 61 .…”

Section: Discussionmentioning

confidence: 73%

Tissue-resident memory T cells in Epicardial adipose tissue comprise transcriptionally distinct subsets that are modulated in Atrial Fibrillation

Longhi,

Vyas,

Sandhar

et al. 2023

Preprint

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Atrial fibrillation (AF) is the most common sustained arrhythmia and carries an increased risk of stroke and heart failure. Here, we investigate how the immune infiltrate of human epicardial adipose tissue (EAT), which directly overlies the myocardium, contributes to AF. Flow cytometry analysis revealed an enrichment of tissue-resident memory T (TRM) cells in AF patients. Cellular indexing of transcriptomes and epitopes by sequencing (CITE-Seq) and single-cell TCR sequencing, identified two transcriptionally distinct CD8+ TRM cells that are modulated in AF. Spatial transcriptomic analysis of EAT and atrial tissue identified the border region between the tissues to be a region of intense inflammatory and fibrotic activity, while the addition of TRM populations to atrial cardiomyocytes demonstrated their ability to differentially alter calcium flux as well as activate inflammatory and apoptotic signalling pathways. This study identified EAT as a novel reservoir of TRM cells that can directly modulate vulnerability to cardiac arrhythmia.

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“…Kinetics of IL‐2‐induced intracellular nitric oxide (NO) production were assessed by the incubation of cardiomyocytes with NO‐sensitive fluorescent dye 4‐amino‐5‐methylamino‐2′,7′‐difluorofluorescein diacetate (DAF‐FM, 5 µmol/L) in 3 mL of standard Kraftbrühe solution for 30 min 20 . Further, cardiomyocytes were washed for 30 min and transferred from suspension to a perfusion chamber where they adhered freely to the glass bottom 21‐24 . 15‐20 min after precipitation, cells were incubated in a standard Kraftbrühe solution containing 2 ng/mL IL‐2.…”

Section: Methodsmentioning

confidence: 99%

“…20 Further, cardiomyocytes were washed for 30 min and transferred from suspension to a perfusion chamber where they adhered freely to the glass bottom. [21][22][23][24] 15-20 min after precipitation, cells were incubated in a standard Kraftbrühe solution containing 2 ng/mL IL-2. Fluorescence (in time intervals of 1, 5, 10, 30, 60 and 120 min) was measured prior to and after IL-2 incubation of the same cell at λex = 495 and λem = 515 nm, respectively.…”

Section: Intracellular No Concentration Assessment By Daf-fm Fluorementioning

confidence: 99%

Cardiomyocytes' prolonged IL‐2 incubation induces enhancement in L‐type Ca²⁺ channels mediated by inhibitory‐kappaB kinase/nuclear factor‐kappaB signalling

Mitrokhin

Горбачева

Vachrushev

et al. 2020

Basic Clin Pharma Tox

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The main objective of this study was to determine the primary intracellular signalling pathway affected by prolonged (2 hours) incubation in interleukin-2 (IL-2). Based on the inflammatory nature of IL-2, priority was given to the involvement of inhibitory-kappaB kinase/nuclear factor-kappaB (IKK/NF-κB) signalling. All of the experiments were performed on freshly prepared cardiomyocytes isolated from rat left ventricles. After isolation, the whole-cell voltage-clamp recordings were performed on single cells. After 2 hours of incubation in IL-2, the current at 0 mV was approximately 100% higher than at the start of the incubation. ACHP, a highly specific kinase β inhibitor, in a concentration of 10 nmol/L, caused significant reduction in the I Ca,L. IL-2 (2 ng/mL) in the presence of 0.1 μmol/L IMD-0354 as a specific inhibitor of IKKβ, caused nearly no changes in the I Ca,L. IL-2 (3 ng/mL) induced a significant increase in phosphorylated NF-κB p65. The cardiomyocytes incubated in a Kraftbrühe solution containing IL-2 plus PDTC as a specific inhibitor of inducible nitric oxide synthase (iNOS) for 2 hours had a similar I Ca,L increase compared to the cells incubated only in IL-2. IL-2-induced enhancement in L-type Ca 2+ channels was mediated by IKK/NF-κB signalling, but not via iNOS-mRNA signalling.

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L-type Ca2+ channels’ involvement in IFN-γ-induced signaling in rat ventricular cardiomyocytes

Cited by 8 publications

References 26 publications

Warmer, faster, stronger: Ca2+ cycling in avian myocardium

Warmer, faster, stronger: Ca2+ cycling in avian myocardium

Tissue-resident memory T cells in Epicardial adipose tissue comprise transcriptionally distinct subsets that are modulated in Atrial Fibrillation

Cardiomyocytes' prolonged IL‐2 incubation induces enhancement in L‐type Ca²⁺ channels mediated by inhibitory‐kappaB kinase/nuclear factor‐kappaB signalling

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L-type Ca2+ channels’ involvement in IFN-γ-induced signaling in rat ventricular cardiomyocytes

Cited by 8 publications

References 26 publications

Warmer, faster, stronger: Ca2+ cycling in avian myocardium

Warmer, faster, stronger: Ca2+ cycling in avian myocardium

Tissue-resident memory T cells in Epicardial adipose tissue comprise transcriptionally distinct subsets that are modulated in Atrial Fibrillation

Cardiomyocytes' prolonged IL‐2 incubation induces enhancement in L‐type Ca2+ channels mediated by inhibitory‐kappaB kinase/nuclear factor‐kappaB signalling

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Cardiomyocytes' prolonged IL‐2 incubation induces enhancement in L‐type Ca²⁺ channels mediated by inhibitory‐kappaB kinase/nuclear factor‐kappaB signalling