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Artigos de revistas sobre o assunto "Canaux BKCa"
Sigouin, Audrey, Marc Bélisle, Dany Garant e Fanie Pelletier. "Agricultural pesticides and ectoparasites: potential combined effects on the physiology of a declining aerial insectivore". Conservation Physiology 9, n.º 1 (1 de janeiro de 2021). http://dx.doi.org/10.1093/conphys/coab025.
Texto completo da fonteTeses / dissertações sobre o assunto "Canaux BKCa"
Ferraguto, Celeste. "BKCa channels as therapeutic targets in neurodevelopmental disorders : focus on acoustic dysfunction". Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0134.
Texto completo da fonteNeurodevelopmental disorders (NDDs) are typically characterized by a range of pathological phenotypes, encompassing a variety of physical, brain, and behavioral abnormalities. Among these, impaired auditory perception and hearing alterations are commonly observed across multiple NDDs. Given the presence of shared symptomatology, increasing interest is devoted to the identification of potential common underlying mechanisms and, therefore, shared therapeutic strategies. Despite extensive efforts, effective pharmacological interventions for most NDDs are still lacking, prompting research on novel drugs, as well as on repurposed treatments. Dysfunction in big conductance calcium-activated potassium (BKCa) ion channels has emerged as a potential key pathological mechanism involved in multiple NDDs: these ubiquitous channels play a pivotal role in modulating the activity of excitable cells, including neurons, vascular smooth muscle, and cardiac cells, as well as cochlear hair cells, thus being strongly implicated in synaptic, cardio-vascular and auditory functions. Notably, reduced expression and functionality of BKCa channels have been documented in patients with two major NDDs, i.e., fragile X and Williams-Beuren syndromes (FXS and WBS), suggesting that compounds activating these channels could offer promising treatments for these two genetic syndromes. This thesis aimed to provide preclinical evidence supporting the therapeutic potential of Chlorzoxazone, an FDA-approved BKCa channel opener, for treating the pathological phenotypes of FXS and WBS. To this end, we employed the Fmr1-KO and the CD mouse lines, representing the main preclinical models of FXS and WBS, respectively, which recapitulate most symptoms displayed by patients, including BKCa channel expression and functional deficits. In the first part of the thesis, we demonstrated that Chlorzoxazone, administered either acutely or chronically, effectively treated various behavioral, brain, and physical phenotypes exhibited by Fmr1-KO and CD mutants. To this aim, we combined behavioral assessments of both mutant mouse lines, encompassing motor, emotional, and social tests, with the analysis of markers of neuronal plasticity and functionality, e.g., dendritic abnormalities, neurotrophin levels, and fos expression in specific brain regions. Additionally, in the CD mouse model, we characterized cardiovascular phenotypes typical of WBS, i.e., cardiac hypertrophy and aortic stenosis. In the second part, we focused on the auditory alterations displayed by the two mouse models and we showed the overall efficacy of Chlorzoxazone in rescuing these abnormalities at electrophysiological, structural, and behavioral levels. This involved assessing auditory brainstem responses and distortion product otoacoustic emissions, alongside the immuno-histochemical evaluation of cochlear hair cells and ribbon synapses, and behavioral analysis of the acoustic startle response. Overall, our findings support BKCa channels as promising therapeutic targets for FXS and WBS, as well as for associated auditory dysfunctions. Furthermore, they advocate for repurposing Chlorzoxazone, already on the market for muscular pathologies, for clinical use in the context of NDDs. In conclusion, this thesis provides a preclinical foundation for future clinical trials in FXS and WBS and encourages further preclinical research into the role of BKCa channels in auditory and behavioral dysfunction
Ambroisine, Marie-Lory. "Mécanismes physiopathologiques de l'aldostérone dans la dysfonction coronaire : rôle des canaux potassiques BKCa et implication du genre". Paris 7, 2007. http://www.theses.fr/2007PA077240.
Texto completo da fonteAldosterone (Aldo) antagonists correct the coronary dysfonction (CD) in human but the mechanisms are less understood. Our team has demonstrated that mice overexpressing thé Aldo synthase (AS) in cardiomyocytes have nitric oxide (NO)-independent coronary dysfonction. We have investigated the potentials mechanisms of the Aldo in CD. This work is constituted in three parts based on several hypotheses. 1. Because the Aldo has an inflammatory effect, we hypothetized that the CD is induced by an inflammatory phénotype. 2. The interactions between endothelial cells and vascular smooth muscle cells (VSMC) are very important in vasodilatation. The CD of AS mice could be the consequence of vascular cell dysfonction. 3. The impact of gender has been also studied. This work enabled us to conclude that there is no inflammatory cell in the pericoronary area of the AS mice ventricles, not the expression of genes of the inflammatory cytokines or the oxidative stress. The study of the coronary reactivity in thé présence of inhibitor or activator of the vasodilatation showed that the fonction of the endothelial cell does not seem to be altered. On thé other hand, the CD of the AS mice is dependent of the calcium-activated potassium channels (BKCa) of thé CMLv as well as hormonal status. In CMLv culture, the inhibitory effect of Aldo on BKCa expression is prevented by the spironolactone and the 17b estradiol. In conclusion, the CD induced by Aldo is independent of the inflammation but dependent of the BKCa and the gender. This work could open towards new therapeutic targets of CD induced by cardiac Aldo
Azhikkattuparambil, Bhaskaran Arjun. "Cellular and circuit mechanisms of neocortical dysfunction in Fragile X Syndrome". Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0244/document.
Texto completo da fonteThis study explores the evoked responses, intrinsic and spontaneous activity of two different neuronal populations in the hind paw region of the primary somatosensory cortex (S1) of mice. Initially, we explored information processing in these neurons under normal physiological conditions, and subsequently in a mouse model of Fragile X Syndrome (FXS). FXS is the most common form of inherited mental retardation syndrome and a frequent cause of autism spectrum disorders (ASD). FXS is a single gene (Fmr1) disorder, which can be reliably modeled by a mutant mouse model, the Fmr1 knockout (Fmr1-/y) mouse. Hyperexcitability of neocortical networks and hypersensibility to sensory stimuli are prominent features of FXS and ASD. We previously established a strong causal link between a channelopathy, hyperexcitability of neurons in the primary sensory region of the neocortex and sensory hypersensitivity in this mouse model. In the current study, we extended these findings, by conducting a detailed exploration of the processing of tactile sensory information (evoked by hind paw stimulation) in the neocortex of these mice.Most of our knowledge regarding information processing in S1 comes from studies of the whisker-related barrel cortex (which processes tactile-related sensory information derived from the whiskers), yet the processing of sensory inputs from the hind-paws is poorly understood. Using in vivo whole-cell patch-clamp recordings, we classified the cells into suprathreshold responders (the cells which responded to the hind-paw stimulations with an action potential), subthreshold responders (the cells responded without eliciting an action potential) and non-responder cells (neurons which did not show any response). We then compared the evoked sub- and supra-threshold responses, intrinsic properties, and spontaneous activity of layer (L) 2/3 pyramidal neurons of the S1 hind-paw (S1-HP) region of anaesthetized wild type (WT) and Fmr1-/y mice. We identified spontaneous, intrinsic and evoked response alterations in Fmr1-/y mice. We probed possible mechanisms contributing to this sensory impairment in Fmr1-/y mice. Finally, we tested the possibility of correcting pathophysiological alterations in these neurons using specific pharmacological agents targeting the ion channel defects described previously by our team
Gambade, Audrey. "Rôle du peptide LL-37 dans le cancer du sein : son interaction avec la membrane plasmique stimule l'entrée de calcium et la migration cellulaire par l'activation des canaux ioniques TRPV2 et BKCa". Thesis, Tours, 2015. http://www.theses.fr/2015TOUR3312/document.
Texto completo da fonteThe antimicrobial peptide LL-37 is overexpressed in several types of cancer, among which breast cancer were it is associated with metastasis development. Our experiments on three mammary cancer cell lines have shown that LL-37 increases cell migration. Both its natural (L)-form and its (D)-enantiomer are equally active, excluding a specific binding to a protein receptor. On the MDA-MB-435s cell line, LL-37 attaches to plasma membrane and reduces its fluidity. Electron microscopy localized LL-37 on the surface of pseudopodia, structures implicated in cell migration, and in caveolae. LL-37 induces calcium entry via the TRPV2 channel, which is recruited to pseudopodia. Recruitment depends on activation of PI3K/AKT signaling induced by LL-37. Calcium entry via TRPV2 is potentiated by activation of the BKCa potassium channel also located in pseudopodia. TRPV2 suppression by RNA interference results in 70% reduction of cell migration induced by LL-37, attributing a crucial role of this channel to the promigratory effects of the peptide. Binding of LL-37 to cancer cell membranes and in consequence the activation of ion channels constitutes a novel research field to understand its role in tumor progression
Ayad, Oualid. "Caractérisation fonctionnelle des cellules souches cardiaques humaines dans un but thérapeutique". Thesis, Poitiers, 2017. http://www.theses.fr/2017POIT2303/document.
Texto completo da fonteThe aim of this thesis was to develop and characterize a model of human heart stem cells in a context of cell therapy.A population of mesenchymal stem cells, expressing the W8B2 marker (CSCs W8B2+), was first isolated from human auricles and characterized using high-throughput RT-qPCR techniques, immuno-labeling, western-blot and calcium fluorescence imaging. These experiments were focused on 1. the gene expression of ion channels and calcium signaling proteins; and 2. the study of CSCs W8B2+ in vitro differentiation and associated intracellular calcium activity changes.The results show that CSCs W8B2+ tend to differentiate into pacemaker cells. Some nodal specific genes such as Tbx3, HCN, ICaT, L, Kv, NCX, are expressed during differentiation. The recording of calcium activity (via an optogenetic probe) shows the presence of calcium oscillations that change in frequency and intensity during differentiation. IP3 sensitive calcium stocks and the NCX exchanger would play a fundamental role in these variations.Then we studied the importance of the BKCa channel and the sphingosine 1-phosphate (S1P) receptors in the regulation of the fundamental properties of the W8B2+ CSCs. Inhibition of BKCa reduces cell proliferation by accumulating cells in the G0 / G1 phase, suppresses cell self-renewal but does not affect migration properties. Concerning S1P, it decreases proliferation and self-renewal without stimulate S1P1,2,3 receptors.This work highlights fundamental potential molecular targets in a context of cardiac cell therapy