A5028288545- Cardiac electrophysiology and arrhythmias
- Ion channel regulation and function
- Neuroscience and Neural Engineering
- Cardiovascular Effects of Exercise
- Receptor Mechanisms and Signaling
- Protein Kinase Regulation and GTPase Signaling
- Cardiac Arrhythmias and Treatments
- Neuroscience and Neuropharmacology Research
- Advanced Fluorescence Microscopy Techniques
- Nitric Oxide and Endothelin Effects
- Nicotinic Acetylcholine Receptors Study
- Signaling Pathways in Disease
- Cardiovascular Function and Risk Factors
- Adipose Tissue and Metabolism
- Connective Tissue Growth Factor Research
- Electron Spin Resonance Studies
- Electrochemical sensors and biosensors
- Trace Elements in Health
- Heavy Metal Exposure and Toxicity
- Computational Drug Discovery Methods
- Cancer, Hypoxia, and Metabolism
- Parathyroid Disorders and Treatments
- Integrated Circuits and Semiconductor Failure Analysis
- RNA Research and Splicing
- Ion Channels and Receptors
University of Bern
2015-2024
Hospital Universitario Virgen del Rocío
2009-2024
Instituto de Biomedicina de Sevilla
2009-2024
Universidad de Sevilla
2009-2024
During β-adrenergic receptor (β-AR) stimulation, phosphorylation of cardiomyocyte ryanodine receptors by protein kinases may contribute to an increased diastolic Ca2+ spark frequency. Regardless prompt activation kinase A during β-AR this appears rely more on Ca2+/calmodulin-dependent II (CaMKII), a not yet identified signalling pathway. The goal the present study was identify and characterize mechanisms which lead CaMKII elevated frequencies stimulation in single cardiomyocytes conditions....
During physical exercise or stress, the sympathetic system stimulates cardiac contractility via β-adrenergic receptor (β-AR) activation, resulting in protein kinase A (PKA)-mediated phosphorylation of ryanodine RyR2. PKA-dependent "hyperphosphorylation" RyR2 channel has been proposed as a major impairment that contributes to progression heart failure. However, sites PKA and their status diseases are not well defined. Among known sites, serine 2030 (S2030) remains highly controversial site...
Background: Sustained vascular smooth muscle contraction is mediated by extracellular Ca 2+ influx through L-type voltage-gated channels (VGCC) and RhoA/Rho-associated kinase (ROCK)-dependent sensitization of the contractile machinery. VGCC activation can also trigger an ion-independent metabotropic pathway that involves G-protein/phospholipase C activation, inositol 1,4,5-trisphosphate synthesis, release from sarcoplasmic reticulum (calcium channel-induced release). We have studied...
The mechanisms controlling differentiation in adult cardiac precursor cells (CPCs) are still largely unknown. In this study, CPCs isolated from the human heart were found to produce predominantly smooth muscle but could be redirected cardiomyocyte fate by transient activation followed inhibition of NOTCH signaling. repressed MIR-143/145 expression, and blocked differentiation. Expression microRNAs is under control CARMEN, a long noncoding RNA associated with an enhancer located locus target...
Rationale: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare disease, manifested by syncope or sudden death in children young adults under stress conditions. Mutations the Ca 2+ release channel/RyR2 (type 2 ryanodine receptor) gene account for about 60% of identified mutations. Recently, we found and described mutation RyR2 N-terminal domain, R420Q . Objective: To determine arrhythmogenic mechanisms this mutation. Methods Results: Ventricular tachycardias conditions were...
The release of Ca
The human zinc transporter SLC39A2, also known as ZIP2, was shown to mediate transport that could be inhibited at pH <7.0 and stimulated by HCO3–, suggesting a Zn2+/HCO3– cotransport mechanism [Gaither, L. A., Eide, D. J. (2000) Biol. Chem. 275, 5560–5564]. In contrast, recent experiments in our laboratory indicated the functional activity of ZIP2 increases acidic [Franz, M. C., et al. (2014) Biomol. Screening 19, 909–916]. study presented here therefore designed reexamine findings about...
In arterial myocytes, membrane depolarization-induced Ca(2+) release (DICR) from the sarcoplasmic reticulum (SR) occurs through a metabotropic pathway that leads to inositol trisphosphate synthesis independently of extracellular influx. Despite fundamental functional relevance DICR, its molecular bases are not well known.Biophysical and pharmacological data have suggested L-type channels could be sensors coupling depolarization SR release. This hypothesis was tested using smooth...
We have previously described in rat basilar arterial myocytes that the absence of extracellular Ca2+ influx, activation L-type channels stimulates a metabotropic cascade leading to release from sarcoplasmic reticulum (SR) and contraction [a calcium channel-induced (CCICR) mechanism]. On other hand, it is known hypoxia reduces channel activity coronary myocytes. In present study, we investigated whether CCICR ring induced by can be inhibited hypoxia. Isometric force, diameter, cytosolic...
Increased protein phosphatase 1 (PP-1) activity has been found in end stage human heart failure. Although PP-1 extensively studied, a detailed understanding of its role the excitation-contraction coupling mechanism, normal and diseased hearts, remains elusive. The present study investigates functional effect on local Ca2+ release events ventricular cardiomyocytes, by using an activating peptide (PDP3) for stimulation endogenous protein. We report that acute de-phosphorylation may increase...
Abstract During exercise or stress, the sympathetic system stimulates cardiac contractility via β‐adrenergic receptor (β‐AR) activation, resulting in phosphorylation of ryanodine (RyR2). Three RyR2 sites have taken prominence excitation–contraction coupling: S2808 and S2030 are described as protein kinase A specific S2814 a Ca 2+ /calmodulin type‐2‐specific site. To examine contribution these phosphosites to signalling, we generated double knock‐in (DKI) mice which Ser2808 Ser2814 both been...
Abstract Background and Objectives Ongoing studies are shedding light on the potential connection between FGF23 hypertension. In experimental settings, administration of recombinant in mice has been demonstrated to induce hypertension by elevating serum sodium, along with an increase NCC receptors kidney. Clinical evidences further supports pro-hypertensive effects high circulating levels FGF23. Our group previously a direct influence increased arterial stiffness inducing phenotypic...