scholarly journals STAT4 silencing underlies a novel inhibitory role of microRNA-141-3p in inflammation response of mice with experimental autoimmune myocarditis

2019 ◽  
Vol 317 (3) ◽  
pp. H531-H540 ◽  
Author(s):  
Aiqun Pan ◽  
Yuying Tan ◽  
Zhihao Wang ◽  
Guoliang Xu
Keyword(s):  
Body Weight ◽  
Cardiac Function ◽  
Weight Ratio ◽  
Heart Weight ◽  
Inflammatory Factor ◽  
Body Weight Ratio ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

As an inflammatory disease afflicting the heart muscle, autoimmune myocarditis (AM) represents one of the foremost causes of heart failure. Accumulating evidence has implicated microRNAs (miRNAs) in the process of inflammation and autoimmunity. Hence, the current study aimed to investigate the mechanism by which miR-141-3p influences experimental AM (EAM). An EAM mouse model was established using 6-wk old male BALB/c mice, after which the expression of miR-141-3p and STAT4 was measured. Gain-of-function and loss-of-function investigations were performed to identify the functional role of miR-141-3p and STAT4 in EAM. Heart weight-to-body weight ratio, cardiac function, and degree of inflammation, as well as the levels of inflammation factors (IFN-γ, TNF-α, IL-2, IL-6, and IL-17) in the serum were detected. STAT4 was subsequently verified to be upregulated, and miR-141-3p was downregulated in the EAM mice. Furthermore, the overexpression of miR-141-3p or silencing of STAT4 was observed to reduce the heart weight-to-body weight ratio of EAM mice and improve cardiac function, while alleviating the degree of inflammatory cell infiltration in the myocardial tissue. Meanwhile, the overexpression of miR-141-3p was identified to diminish serum inflammatory factor levels by downregulating STAT4. Additionally, miR-141-3p could bind to STAT4 to downregulate its expression, ultimately mitigating inflammation and inducing an anti-inflammatory effect in EAM mice. Taken together, upregulation of miR-141-3p alleviates the inflammatory response in EAM mice by inhibiting STAT4, providing a promising intervention target for the molecular treatment of AM. NEW & NOTEWORTHY miR-141-3p is poorly expressed, and STAT4 is upregulated in experimental autoimmune myocarditis (EAM) mice. Overexpressing miR-141-3p inhibits EAM. miR-141-3p binds to and suppresses STAT4 expression. miR-141-3p overexpression inhibits inflammatory factors by downregulating STAT4. This study provides new insights into the treatment of autoimmune myocarditis.

scholarly journals Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1267 ◽  
Author(s):  
Ludwig T. Weckbach ◽  
Andreas Uhl ◽  
Felicitas Boehm ◽  
Valentina Seitelberger ◽  
Bruno C. Huber ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Ratio ◽  
Heart Weight ◽  
Lymphocyte Function ◽  
Body Weight Ratio ◽  
Antibody Treatment ◽  
Autoimmune Myocarditis ◽  
Cardiac Inflammation ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

The lymphocyte function-associated antigen 1 (LFA-1) is a member of the beta2-integrin family and plays a pivotal role for T cell activation and leukocyte trafficking under inflammatory conditions. Blocking LFA-1 has reduced or aggravated inflammation depending on the inflammation model. To investigate the effect of LFA-1 in myocarditis, mice with experimental autoimmune myocarditis (EAM) were treated with a function blocking anti-LFA-1 antibody from day 1 of disease until day 21, the peak of inflammation. Cardiac inflammation was evaluated by measuring infiltration of leukocytes into the inflamed cardiac tissue using histology and flow cytometry and was assessed by analysis of the heart weight/body weight ratio. LFA-1 antibody treatment severely enhanced leukocyte infiltration, in particular infiltration of CD11b+ monocytes, F4/80+ macrophages, CD4+ T cells, Ly6G+ neutrophils, and CD133+ progenitor cells at peak of inflammation which was accompanied by an increased heart weight/body weight ratio. Thus, blocking LFA-1 starting at the time of immunization severely aggravated acute cardiac inflammation in the EAM model.

scholarly journals Quercetin Ameliorates Experimental Autoimmune Myocarditis in Rats

2010 ◽  
Vol 13 (3) ◽  
pp. 311 ◽  
Author(s):  
Marina Milenković ◽  
Nevena Arsenović-Ranin ◽  
Zorica Stojić-Vukanić ◽  
Biljana Bufan ◽  
Dragana Vučićević ◽  
...  
Keyword(s):  
Histopathological Examination ◽  
Weight Ratio ◽  
Heart Weight ◽  
Tnf Alpha ◽  
Dark Agouti ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Anti Inflammatory ◽  
Culture Supernatants ◽  
Experimental Autoimmune

Purpose: Experimental autoimmune myocarditis (EAM) in rats is an animal model of human giant cell myocarditis and post-myocarditis dilated cardiomyopathy. The pathogenesis of EAM has not been elucidated, but there is accumulating evidence that cytokines secreted from monocytes/macrophages and T cells play a crucial role in the induction and progression of disease. Flavonoids are a large group of polyphenolic compounds abundantly present in the human diet, which scavenge oxygen radicals and have anti-inflammatory activities. Having in mind in vivo beneficial effects of flavonoid quercetin in different animal models of immunoinflammatory diseases such as experimental autoimmune encephalomyelitis and adjuvant arthritis, on the one side, and its in vitro suppressive effect on production of tumor necrosis factor–alpha (TNF-alpha on the other side, we investigated the effects of quercetin on EAM in rats. Methods: Myocarditis was induced in Dark Agouti (DA) rats by injection of porcine cardiac myosin and quercetin at doses of 10 or 20 mg/kg was orally administered from days 0 to 21 after induction of disease. The severity of myocarditis was evaluated by determination of heart weight / body weight ratio (Hw/Bw) and histopathological examination of hearts. The levels of cytokines (TNF-alpha, IL-12, IL-17 and IL-10) in serum and lymph node cells (LNC) culture supernatants were measured by ELISA. Results: The rats treated with 20 mg/kg of quercetin had significantly decreased incidence of EAM, Hw/Bw, macroscopic and microscopic scores of hearts. Further, in EAM rats treated with quercetin levels of TNF-alpha and IL-17 were significantly lower, while the level of IL-10 was significantly higher both in serum and culture supernatants of LNC stimulated with concanavalin A compared with vehicle-treated animals. Conclusions: The present study suggests that quercetin ameliorates EAM, at least in part, by interfering production of proinflammatory (TNF-alpha and IL-17) and/or anti-inflammatory (IL-10) cytokines.

Inhibition of NF-κB activation by a novel IKK inhibitor reduces the severity of experimental autoimmune myocarditis via suppression of T-cell activation

2013 ◽  
Vol 305 (12) ◽  
pp. H1761-H1771 ◽  
Author(s):  
Ryo Watanabe ◽  
Ryoko Wakizono Azuma ◽  
Jun-ichi Suzuki ◽  
Masahito Ogawa ◽  
Akiko Itai ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Weight Ratio ◽  
Heart Weight ◽  
Autoimmune Myocarditis ◽  
Inflammatory Reactions ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

NF-κB, which is activated by the inhibitor of NF-κB kinase (IKK), is involved in the progression of inflammatory disease. However, the effect of IKK inhibition on the progression of myocarditis is unknown. We examined the effect of IKK inhibition on the progression of myocarditis. Lewis rats were immunized with porcine cardiac myosin to induce experimental autoimmune myocarditis (EAM). We administered the IKK inhibitor (IMD-0354; 15 mg·kg−1·day−1) or vehicle to EAM rats daily. Hearts were harvested 21 days after immunization. Although the untreated EAM group showed increased heart weight-to-body weight ratio, and severe myocardial damage, these changes were attenuated in the IKK inhibitor-treated group. Moreover, IKK inhibitor administration significantly reduced NF-κB activation and mRNA expression of IFN-γ, IL-2, and monocyte chemoattractant protein-1 in myocardium compared with vehicle administration. In vitro study showed that the IKK inhibitor treatment inhibited T-cell proliferation and Th1 cytokines production induced by myosin stimulation. The IKK inhibitor ameliorated EAM by suppressing inflammatory reactions via suppression of T-cell activation.

scholarly journals IL-17 Upregulates MCP-1 Expression via Act1 / TRAF6 / TAK1 in Experimental Autoimmune Myocarditis

2021 ◽  
Author(s):  
xiao huang ◽  
Zhuolun Li ◽  
Xinhe Shen ◽  
na nie ◽  
yan shen
Keyword(s):  
Myocardial Tissue ◽  
Inflammatory Factor ◽  
Mononuclear Cell Infiltration ◽  
Autoimmune Myocarditis ◽  
Inflammatory Infiltration ◽  
Mrna And Protein Expression ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune ◽  
Important Cytokine

Abstract Myocarditis is a myocardial inflammatory infiltration heterogeneous disease. At present, various interventions are not effective in the treatment of myocarditis. IL-17, an important pro‐inflammatory factor secreted mainly by Th17 cells, can promote the expression of multiple cytokines. MCP-1 is an important cytokine that mediates mononuclear cell infiltration. Studies have found that IL-17 could stimulate the expression of MCP-1 to mediate inflammatory infiltration. But the mechanism by which IL-17 induces MCP-1 expression in experimental autoimmune myocarditis (EAM) remains unclear. The purpose of this study is to establish an EAM model to explore the role of Act1/TRAF6/TAK1 cascade in the induction of MCP-1 by IL-17. In the present study, we found that in EAM, IL-17 could stimulate the expression of MCP-1 by activating Act1/TRAF6/TAK1 cascade. After interfering TAK1 with si-TAK1, myocardial tissue inflammation was greatly alleviated, and both MCP-1 mRNA and protein expression were downregulated. In conclusion, IL-17 can activate AP-1, NF-κB via Act1/TRAF6/TAK1 upregulation of MCP-1 expression in EAM.

scholarly journals Cardiac hypertrophy associated with impaired regulation of cardiac ryanodine receptor by calmodulin and S100A1

2013 ◽  
Vol 305 (1) ◽  
pp. H86-H94 ◽  
Author(s):  
Naohiro Yamaguchi ◽  
Asima Chakraborty ◽  
Tai-Qin Huang ◽  
Le Xu ◽  
Angela C. Gomez ◽  
...  
Keyword(s):  
Body Weight ◽  
Amino Acid ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Ryanodine Receptor ◽  
Weight Ratio ◽  
Heart Weight ◽  
Mrna Levels ◽  
Body Weight Ratio

The cardiac ryanodine receptor (RyR2) is inhibited by calmodulin (CaM) and S100A1. Simultaneous substitution of three amino acid residues (W3587A, L3591D, F3603A; RyR2ADA) in the CaM binding domain of RyR2 results in loss of CaM inhibition at submicromolar (diastolic) and micromolar (systolic) Ca2+, cardiac hypertrophy, and heart failure in Ryr2 ADA/ADA mice. To address whether cardiac hypertrophy results from the elimination of CaM and S100A1 inhibition at diastolic or systolic Ca2+, a mutant mouse was generated with a single RyR2 amino acid substitution (L3591D; RyR2D). Here we report that in single-channel measurements RyR2-L3591D isolated from Ryr2 D/D hearts lost CaM inhibition at diastolic Ca2+ only, whereas S100A1 regulation was eliminated at both diastolic and systolic Ca2+. In contrast to the ∼2-wk life span of Ryr2 ADA/ADA mice, Ryr2 D/D mice lived longer than 1 yr. Six-month-old Ryr2 D/D mice showed a 9% increase in heart weight-to-body weight ratio, modest changes in cardiac morphology, and a twofold increase in atrial natriuretic peptide mRNA levels compared with wild type. After 4-wk pressure overload with transverse aortic constriction, heart weight-to-body weight ratio and atrial natriuretic peptide mRNA levels increased and echocardiography showed changes in heart morphology of Ryr2 D/D mice compared with sham-operated mice. Collectively, the findings indicate that the single RyR2-L3591D mutation, which distinguishes the effects of diastolic and systolic Ca2+, alters heart size and cardiac function to a lesser extent in Ryr2 D/D mice than the triple mutation in Ryr2 ADA/ADA mice. They further suggest that CaM inhibition of RyR2 at systolic Ca2+ is important for maintaining normal cardiac function.

scholarly journals Activated myofibroblasts promote cardiac hypertrophy and systolic dysfunction independently of cardiac fibrosis in experimental autoimmune myocarditis

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
K Tkacz ◽  
A Jazwa-Kusior ◽  
F Rolski ◽  
E Dzialo ◽  
K Weglarczyk ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Dilated Cardiomyopathy ◽  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Systolic Dysfunction ◽  
Heart Weight ◽  
Type I ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Abstract Background/Introduction Heart-specific inflammation – myocarditis is a common cause dilated cardiomyopathy which is characterized by pathological tissue remodeling, ventricular stiffening, cardiomyopathy and heart failure. In experimental autoimmune myocarditis (EAM) susceptible mice immunized with alpha myosin heavy chain (αMyHC) and complete Freund's adjuvant (CFA) develop acute myocarditis driven by autoreactive CD4+ T cells that is followed by progressive fibrosis, cardiomyopathy and systolic dysfunction. Purpose The aim of the study was to investigate the role of cardiac fibroblasts and myofibroblasts in myocarditis and post-inflammatory dilated cardiomyopathy in mouse model of EAM. Methods EAM was induced in BALB/c mice by immunization with αMyHC/CFA. We used reporter mice expressing EGFP under collagen type I promoter (Coll-EGFP) and RFP under a control of α-smooth muscle actin (αSMA) promoter (αSMA-RFP) and transgenic αSMA-TK mice with ganciclovir-inducible ablation of proliferating myofibroblasts. Cardiac cells were quantified using flow cytometry. Cardiac fibroblasts (CD45-CD31-EGFP+) were sorted from healthy and myocarditis-positive (day 21) mice using BD FACSAria™ II Cell Sorter and analyzed for the whole genome transcriptomics by RNA sequencing. Echocardiography was performed on Vevo 2100 Imaging System. Cardiac fibrosis was assessed by Trichrome Massons's staining and hydroxyproline assay, whereas cardiac hypertrophy by analysing cross-sectional cardiomyocyte area. Profibrotic gene expression was assessed by qRT-PCR. Results The total number of cardiac fibroblasts (CD45-CD31-EGFP+) and the subset of myofibroblasts (CD45-CD31-EGFP+RFP+) remained unchanged at inflammatory (d21) and fibrotic stages (d40). Analysis of differentially expressed genes (min. 2x fold change, p value <0.05) pointed out activation of immune processes (mainly chemokine production), response to stress, cytoskeletal and extracellular matrix re-organization in cardiac fibroblasts in response to myocarditis. αSMA-TK mice treated with ganciclovir (from day 21) showed comparable percent of fibrotic area, but significantly reduced heart weight, decreased cardiomyocyte hypertrophy and improved ejection fraction and cardiac output at day 40 comparing to PBS-treated mice. Ganciclovir-treated mice showed also attenuated cardiac Acta2 and Srf but markedly enhanced Mmp2 expression. Conclusions In EAM model cardiac fibroblasts actively participate in proinflammatory and profibrotic responses, while activated myofibroblasts contribute to dilated cardiomyopathy development independently of cardiac fibrosis. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Science Centre (Poland)

Exercise conditioning increases rat myocardial calcium uptake

1986 ◽  
Vol 60 (5) ◽  
pp. 1673-1679 ◽  
Author(s):  
S. N. Levine ◽  
G. T. Kinasewitz
Keyword(s):  
Body Weight ◽  
Sarcoplasmic Reticulum ◽  
Adrenergic Receptors ◽  
Calcium Uptake ◽  
Myocardial Hypertrophy ◽  
Weight Ratio ◽  
Heart Weight ◽  
Scatchard Analysis ◽  
Body Weight Ratio ◽  
Female Wistar Rats

To investigate potential mechanisms underlying the enhanced myocardial performance consequent to exercise training, the adrenergic receptors of myocardial tissue and Ca2+ uptake into sarcoplasmic reticulum-enriched fractions from exercise conditioned animals were compared with that of sedentary controls. Female Wistar rats were exercised by swimming 30 min (5 days/wk) for 12 wk. Exercise conditioning was effective in producing myocardial hypertrophy, as reflected by an increase in heart weight (1.179 +/- 0.022 vs. 1.031 +/- 0.020 g, P less than 0.001) and heart weight-to-body weight ratio (3.29 +/- 0.06 vs. 2.77 +/- 0.05 X 10(-3), P less than 0.001) but no difference in body weight. Despite the myocardial hypertrophy, neither the affinity nor the density of the alpha 1-adrenergic receptors or the beta-adrenergic receptors determined by Scatchard analysis of the ligands [3H]prazosin and [3H]dihydroalprenolol were significantly different between the two groups. The basal Ca2+ uptake into the sarcoplasmic reticulum was also similar (9.90 +/- 0.97 vs. 9.04 +/- 0.75 nmol/mg protein/min), but the addition of calmodulin produced a significantly greater increment in Ca2+ uptake into sarcoplasmic reticulum from the exercised-conditioned animals (1.90 +/- 0.23 vs. 1.21 +/- 0.19 nmol/mg protein/min, P less than 0.03). The adenosine triphosphatase (ATPase) activities of the sarcoplasmic reticulum-enriched fractions of the two groups were similar. We conclude that exercise conditioning produces an enhancement of calmodulin-mediated calcium uptake that is independent of any effect on Ca2+-ATPase.

P6284The antioxidant MitoQ protects against intestinal disturbances in the experimental autoimmune model of myocarditis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
I Gallardo ◽  
B Gutierrez ◽  
M Hernandez ◽  
I Cabero ◽  
Y Alvarez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Weight Ratio ◽  
Heart Weight ◽  
Preclinical Model ◽  
Myeloperoxidase Activity ◽  
Gut Health ◽  
Barrier Dysfunction ◽  
Autoimmune Myocarditis ◽  
Fatty Acid Binding ◽  
Experimental Autoimmune

Abstract Purpose Myocarditis and dilated cardiomyopathy represent the acute and chronic phases of an inflammatory disease of the myocardium, for which no standardized treatment is currently available in clinical practice. Myocardial fibrosis an oxidative stress are pathogenic factors associated with these processes. However, new research has found that gut health can be linked to some cardiac conditions. Thus, in this study we investigated whether intestinal disturbances are present in myocarditis, using a murine experimental autoimmune model (EAM) that mimics human myocarditis, as well as the potential beneficial effect of treatment with the mitochondrial antioxidant, MitoQ. Methods and results EAM was induced in BALB/c mice with a myocardiogenic peptide and mice were treated with MitoQ (50 mg/kg/day, i.p). On day 21 (acute phase), we assessed signs of heart injury (e.g. hypertrophy, fibrosis, oxidative stress) and parameters related to gut damage such as accumulation of reactive oxigen species (superoxide anion: O2·−), inflammation (IL-1β, IL-33, TNFα), microbial translocation (sCD14; intestinal fatty acid binding protein, I-FABP) and mucins in serum and/or intestine. MitoQ teatment significantly reduced the high heart weight/body weight ratio (HW/BW) of EAM mice, a characteristic hallmark of cardiac hyperthropy. Histological analysis of hearts showed presence of fibrosis (Sirius Red stain) and high O2·− levels (DHE stain) in EAM mice whereas these effects were not detectable in cardiac tissue from healthy or MitoQ-treated EAM mice. In addition, the enhanced O2·− ions (DHE stain) and mucin loss (Alcian Blu/PAS stain) found in colon, ileum, jejunum and duodenum sections from EAM mice were attenuated by MitoQ treatment. The systemic markers associated to intestinal barrier disruption, sCD14 and I-FABP, were found strongly increased in serum from EAM mice, and MitoQ prevents this rise. The beneficial MitoQ effects were also associated with a decrease in the pro-inflammatory cytokines TNFα, IL-33 and IL-1β, both in serum and colonic tissue of treated-EAM mice, as well as a reduction of the myeloperoxidase activity in colon, compared with untreated EAM mice. Conclusion Our data show that in addition to the heart, the intestinal tissue is also damaged in the preclinical model of experimental autoimmune myocarditis, and that MitoQ treatment could reverse this profile. Since there are systemic markers released from the intestine, therapeutic strategies targeting to prevent the intestinal oxidative stress and its associated gut barrier dysfunction, could contribute to the amelioration of the disease. Acknowledgement/Funding SAF2016-81063; CIBERCV

1272Effect of age, genetic background and experimental conditions on left atrial monophasic action potential duration, effective refractory period and activation time in Langendorff-perfused murine hearts

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
J Obergassel ◽  
S N Kabir ◽  
M O"reilly ◽  
L C Sommerfeld ◽  
C O"shea ◽  
...  
Keyword(s):  
Body Weight ◽  
Action Potential ◽  
Genetic Background ◽  
Left Atrial ◽  
Coronary Flow ◽  
Weight Ratio ◽  
Monophasic Action Potential ◽  
Heart Weight ◽  
Body Weight Ratio ◽  
Experimental Conditions

Abstract Funding Acknowledgements Supported by EU [CATCH ME] 633196, British Heart Foundation FS/13/43/30324, AA/18/2/34218 LF, PK, DFG FA413 LF, Studienstiftung to JO. Background Studying cardiac electrophysiology in isolated perfused beating murine hearts is a well-established method. The range of normal values for left atrial action potential durations (LA-APD), activation times (LA-AT) and effective refractory periods (atrial ERP) in murine wildtype (WT) is not well known. Purpose This study aimed to establish reference values for LA-APD, LA-AT and atrial ERP and to identify factors that influence these electrophysiological parameters in wildtype (WT) mice. Method We combined results from isolated beating heart Langendorff experiments carried out in WT between 2005 and 2019 using an octopolar catheter inserted into the right atrium and a monophasic action potential electrode recording from the LA epicardium. Electrophysiological parameters (LA-APD at 50%, 70%, 90% repolarization (APD50, APD70, APD90), LA-AT and atrial ERP) at different pacing cycle lengths (PCL) were summarized. We analyzed effects of PCL, genetic background, age, gender, heart weight to body weight ratio (HW/BW), LA weight to body weight ratio (LAW/BW) as well as coronary flow and temperature as experimental conditions. Results Electrophysiological parameters from 222 isolated hearts (114 female, mean age 6.6 ± 0.25 months, range 2.47-17.7 months) of different backgrounds (77 C57BL/6, 23 FVB/N, 33 MF1, 69 129/Sv and 20 Swiss agouti) were combined. Coronary flow rate, flow temperature and start of isolation to cannulation time were constant experimental conditions over the timespan of experiments. LA-APD was longer while LA-AT decreased with longer PCL throughout all genetic backgrounds (Figure 1A). Genetic background showed strong effects on all electrophysiological parameters. LA activation was delayed in 129/Sv compared to other backgrounds (Figure 1D). LA-APD70 and atrial ERP were significantly shorter in Swiss agouti background compared to others. LA-APD70 was also significantly prolonged in 129/Sv background compared to MF1 (Figure 1C). Atrial ERP was longer in FVB/N compared to other backgrounds. Age effects were compared in groups. Atrial ERP was significantly longer in mice ≤ 3 months compared to all older mice. Atrial ERP was also significantly prolonged (+ 3.4ms, + 13.5%) in female mice compared to males (Figure 1B). Conclusion This dataset summarizes left atrial electrophysiological parameters in the beating mouse heart and can serve as a reference for design and interpretation of electrophysiological experiments in murine models of commonly used genetic backgrounds. We confirm that cycle length, genetic background, age and gender affect atrial electrophysiological parameters. Awareness of these will support successful experimental design. Abstract Figure 1

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