A5089826040- Cardiac electrophysiology and arrhythmias
- Atrial Fibrillation Management and Outcomes
- Angiogenesis and VEGF in Cancer
- Nitric Oxide and Endothelin Effects
- Cardiac Arrhythmias and Treatments
- Chemokine receptors and signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- S100 Proteins and Annexins
- Extracellular vesicles in disease
- Atherosclerosis and Cardiovascular Diseases
- Ion channel regulation and function
- Cardiovascular Function and Risk Factors
- Receptor Mechanisms and Signaling
- Cardiovascular Disease and Adiposity
- Anodic Oxide Films and Nanostructures
- Adipose Tissue and Metabolism
- Cancer, Hypoxia, and Metabolism
- Cancer, Stress, Anesthesia, and Immune Response
- Immune cells in cancer
- Corrosion Behavior and Inhibition
- Cardiac Imaging and Diagnostics
- RNA regulation and disease
- Proteoglycans and glycosaminoglycans research
- Inflammatory mediators and NSAID effects
- Nuclear Receptors and Signaling
Inserm
2008-2023
Centre Hospitalier Universitaire de Bordeaux
2023
Université de Bordeaux
2017-2023
Electrophysiology and Heart Modeling Institute
2019-2023
Centre de Recherche Cardio-Thoracique de Bordeaux
2023
Institut de Chimie et des Matériaux Paris-Est
2023
Bibliothèque Nationale de France
2023
Physiologie et Médecine Expérimentale du Coeur et des Muscles
2023
Centre de Résonance Magnétique des Systèmes Biologiques
2023
University of Oxford
2014-2021
Adiponectin has anti-inflammatory effects in experimental models, but its role the regulation of myocardial redox state humans is unknown. Although adiponectin released from epicardial adipose tissue (EpAT), it unclear whether exerts any paracrine on human myocardium.To explore cross talk between EpAT-derived and heart.EpAT atrial myocardium were obtained 306 patients undergoing coronary artery bypass grafting. Functional genetic polymorphisms that increase ADIPOQ expression (encoding...
We hypothesized that microparticles (MPs) released after ischemia are endogenous signals leading to postischemic vasculogenesis.MPs from mice ischemic hind-limb muscle were detected by electron microscopy 48 hours unilateral femoral artery ligation as vesicles of 0.1- 1-microm diameter. After isolation sequential centrifugation, flow cytometry analyses showed the annexin V(+) MP concentration was 3.5-fold higher in calves than control muscles (1392+/-406 versus 394+/-180 MPs per 1 mg;...
Objective— Leukocyte infiltration in ischemic areas is a hallmark of myocardial infarction, and overwhelming innate immune cells has been shown to promote adverse remodeling cardiac rupture. Recruitment inflammatory the heart depends highly on family CC-chemokines their receptors. Here, we hypothesized that chemokine decoy receptor D6, which specifically binds scavenges CC-chemokines, might limit inflammation after infarction. Methods Results— D6 was expressed human murine infarcted...
Atrial fibrillation (AF) is a growing public health burden, and its treatment remains challenge. AF leads to electrical remodeling of the atria, which in turn promotes maintenance resistance treatment. Although has long been therapeutic target AF, causes remain poorly understood. We show that atrial-specific up-regulation microRNA-31 (miR-31) goat human depletes neuronal nitric oxide synthase (nNOS) by accelerating mRNA decay alters nNOS subcellular localization repressing dystrophin...
Background— CD4 + and CD8 T lymphocytes are key regulators of postischemic neovascularization. T-cell activation is promoted by 2 major costimulatory signalings, the B7/CD28 CD40–CD40 ligand pathways. Interestingly, CD28 interactions with structurally related ligands B7-1 B7-2 also required for generation homeostasis CD25 regulatory cells (Treg cells), which play a critical role in suppression immune responses control homeostasis. We hypothesized that Treg cell may modulate...
Background— The hypoxia-inducible transcription factor (HIF) subunits are destabilized via the O 2 -dependent prolyl hydroxylase domain proteins (PHD1, PHD2, and PHD3). We investigated whether inhibition of PHDs upregulating HIF might promote postischemic neovascularization. Methods Results— Mice with right femoral artery ligation were treated, by in vivo electrotransfer, plasmids encoding for an irrelevant short hairpin RNA (shRNA) (shCON [control]) or specific shRNAs directed against...
Monocyte systemic levels are known to be a major determinant of ischaemic tissue revascularization, but the mechanisms mediating mobilization different monocyte subsets—Ly6Chi and Ly6Clo—to blood their respective role in post-ischaemic neovascularization not clearly understood. Here, we hypothesized that distinct chemokine/chemokine receptor pathways, namely CCL2/CCR2, CX3CL1/CX3CR1, CCL5/CCR5, differentially control subset levels, might thus impact vessel growth. In model murine hindlimb...
Interaction with heparan sulfate proteoglycans is supposed to provide chemokines the capacity immobilize on cell surface and extracellular matrix for accomplishing both tissue homing signaling of attracted cells. However, consequences exclusive invalidation such interaction roles played by endogenous in vivo remain unascertained.We engineered a mouse carrying Cxcl12 gene (Cxcl12(Gagtm)) mutation that precludes interactions structures while not affecting CXCR4-dependent CXCL12 isoforms (α, β,...
C/EBP homologous protein-10 (CHOP-10) is a novel developmentally regulated nuclear protein that emerges as critical transcriptional integrator among pathways regulating differentiation, proliferation, and survival. In the present study, we analyzed role of CHOP-10 in postnatal neovascularization.Ischemia was induced by right femoral artery ligation wild-type CHOP-10(-/-) mice. capillary structure skeletal muscle, mRNA levels were upregulated ischemia diabetes mellitus. Angiographic score,...
Background Nitric oxide synthase uncoupling occurs under conditions of oxidative stress modifying the enzyme's function so it generates superoxide rather than nitric oxide. with chronic pressure overload, and both are ameliorated by exogenous tetrahydrobiopterin ( BH 4)—a cofactor required for normal function—supporting a pathophysiological link. Genetically augmenting 4 synthesis in endothelial cells fails to replicate this benefit, indicating that other cell types dominate effects...
Abstract Aims Gp91-containing NADPH oxidases (NOX2) are a significant source of myocardial superoxide production. An increase in NOX2 activity accompanies atrial fibrillation (AF) induction and electrical remodelling animal models predicts incident AF humans; however, direct causal role for has not been demonstrated. Accordingly, we investigated whether overexpression mice (NOX2-Tg) is sufficient to generate favourable substrate further assessed the effects atorvastatin, an inhibitor NOX2,...
Brugada syndrome is a significant cause of sudden cardiac death (SCD), but the underlying mechanisms remain hypothetical. This study aimed to elucidate this knowledge gap through detailed ex vivo human heart studies. A was obtained from 15-year-old adolescent boy with normal electrocardiogram who experienced SCD. Postmortem genotyping performed, and clinical examinations were done on first-degree relatives. The right ventricle optically mapped, followed by high-field magnetic resonance...
Objective— Catecholamines have been shown to control bone marrow (BM)–derived cell egress, yet the cellular and molecular mechanisms involved in this effect their subsequent participation postischemic vessel growth are poorly understood. Methods Results— Tyrosine hydroxylase mRNA levels, as well dopamine (DA) norepinephrine (NE) contents, were increased ischemic BM of mice with right femoral artery ligation. Angiographic score, capillary density, arteriole number markedly by treatments DA...
In diabetic patients, heart failure with predominant left ventricular (LV) diastolic dysfunction is a common complication for which there no effective treatment. Oxidation of the NOS (nitric oxide synthase) cofactor tetrahydrobiopterin (BH4) and dysfunctional activity have been implicated in pathogenesis vascular cardiomyopathic phenotype.Using mice models human myocardial samples, we evaluated whether by mechanism increasing BH4 availability prevented or reversed LV induced diabetes.In...
Background: Atrial fibrillation is the most sustained form of arrhythmia in human population that leads to important electrophysiological and structural cardiac remodeling as it progresses into a chronic form. Calcium an established key player cellular electrophysiology heart, yet date, there no information maps calcium signaling across left atrium. Objective: The aim this study determine whether homogenous throughout different regions This work tests hypothesis differences healthy atrium...
Cardiac excitation-contraction coupling can be different between regions of the heart. Little is known at atria level, specifically in left atrium. This important given role cardiac myocytes from pulmonary vein sleeves, which are responsible for ectopic activity during atrial fibrillation. In this study, we present a new method to isolate four atrium large animal model, sheep, highly relevant humans. Using collagenase/protease obtained calcium-tolerant epicardium, endocardium, free wall and...
Introduction: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and associated with increased mortality morbidity. The Exchange Protein directly Activated by cAMP (EPAC), has been implicated in pro-arrhythmic signaling pathways atria, but underlying mechanisms remain unknown. Methods: In this study, we investigated involvement of EPAC1 EPAC2 isoforms genesis AF wild type (WT) mice knockout (KO) for or EPAC2. We also employed EPAC pharmacological modulators to...
<h3>Introduction</h3> Diabetes mellitus (DM) is an important risk factor for atrial fibrillation (AF) – the most common heart rhythm disorder. However, mechanisms underlying this association are poorly understood. In addition, patients with DM often have comorbidities, such as obesity, hypertension, dyslipidaemia, that also independently associated increased AF. The aim of project was to explore whether prolonged hyperglycaemia alone sufficient increase <h3>Methods</h3> Multiple low-dose (50...
Purpose: Understanding the mechanism underlying atrial electrical remodelling in AF is of fundamental importance for prevention and treatment AF. We have recently found that neuronal nitric oxide synthase (nNOS) activity dramatically reduced myocytes from patients with Whether loss nNOS contributes to AF-induced remains be established. Methods: Whole-cell patch clamp was used record action potentials (APs) ion currents human murine right myocytes. induced isoflurane anaesthetised mice by...