A5006098350- Ion channel regulation and function
- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Myasthenia Gravis and Thymoma
- Neurogenesis and neuroplasticity mechanisms
- Neuroscience and Neural Engineering
- Alzheimer's disease research and treatments
- Nerve injury and regeneration
- Wnt/β-catenin signaling in development and cancer
- 3D Printing in Biomedical Research
- Pluripotent Stem Cells Research
- Ion Channels and Receptors
- Biochemical effects in animals
- Stress Responses and Cortisol
- Neuroendocrine regulation and behavior
- MicroRNA in disease regulation
- Muscle Physiology and Disorders
- Cardiomyopathy and Myosin Studies
- Neurotransmitter Receptor Influence on Behavior
- Medicinal Plant Pharmacodynamics Research
- Adipose Tissue and Metabolism
- Memory and Neural Mechanisms
- Diet and metabolism studies
- Receptor Mechanisms and Signaling
- Pharmacological Receptor Mechanisms and Effects
Leiden University Medical Center
2023-2024
Czech Academy of Sciences, Institute of Experimental Medicine
2008-2021
Neuroscience Institute
2017-2020
University of Turin
2017
Czech Academy of Sciences
2008-2016
Charles University
2008-2012
The polymodal transient receptor potential vanilloid 4 (TRPV4) channel, a member of the TRP channel family, is calcium-permeable cationic that gated by various stimuli such as cell swelling, low pH and high temperature. Therefore, TRPV4-mediated calcium entry may be involved in neuronal glia pathophysiology associated with disorders central nervous system, ischemia. TRPV4 has been recently found adult rat cortical hippocampal astrocytes; however, its role astrocyte still not defined. In...
Modulating endogenous regenerative processes may represent a suitable treatment for central nervous system (CNS) injuries, such as stroke or trauma. Neural stem/progenitor cells (NS/PCs), which naturally reside in the subventricular zone (SVZ) of adult brain, proliferate and differentiate to other cell types, therefore compensate negative consequences ischemic injury. The fate NS/PCs developing brain is largely influenced by Wingless/Integrated (Wnt) signaling; however, its role...
Abstract Energy depletion during ischemia leads to disturbed ionic homeostasis and accumulation of neuroactive substances in the extracellular space, subsequently leading volume changes astrocytes. Confocal microscopy combined with 3D reconstruction was used quantify ischemia‐induced astrocyte cortical slices GFAP/EGFP transgenic mice. Twenty‐minutes oxygen‐glucose deprivation (OGD) or acidification (OGD pH 6.8 ) revealed presence two distinct astrocytic populations, first showing a large...
Astrocytes respond to ischemic brain injury by proliferation, the increased expression of intermediate filaments and hypertrophy, which results in glial scar formation. In addition, they alter ion channels, receptors transporters that maintain ionic/neurotransmitter homeostasis. Here, we aimed demonstrate Hcn1-4 genes encoding hyperpolarization-activated cyclic nucleotide-gated (HCN) channels reactive astrocytes following focal cerebral ischemia (FCI) or global (GCI) characterize their...
Brain edema accompanying ischemic or traumatic brain injuries, originates from a disruption of ionic/neurotransmitter homeostasis that leads to accumulation K+ and glutamate in the extracellular space. Their increased uptake, predominantly provided by astrocytes, is associated with water influx via aquaporin-4 (AQP4). As removal perivascular AQP4 deletion α-syntrophin was shown delay formation clearance, we aimed elucidate impact knockout on volume changes individual astrocytes situ evoked...
During the last decade, much progress has been made in developing protocols for differentiation of human embryonic stem cells (hESCs) into a neural phenotype. The appropriate agent cell therapy is precursors (NPs). Here, we demonstrate derivation highly enriched and expandable populations proliferating NPs from CCTL14 line hESCs. These could differentiate vitro functionally active neurons, as confirmed by immunohistochemical staining electrophysiological analysis. Neural differentiated hESCs...
Adherent, fibroblastic cells from different tissues are thought to contain subsets of tissue-specific stem/progenitor (often called mesenchymal stem cells). These display similar cell surface characteristics based on their nature, but also exhibit differences in molecular phenotype, growth rate, and ability differentiate into various phenotypes. The mechanisms underlying these remain poorly understood. We analyzed Ca2 + signals membrane properties rat adipose-derived stromal (ADSCs) bone...
The mechanism of tau toxicity is still unclear. Here we report that recombinant oligomers and monomers, intraventricularly injected in mice with a pure human background, foster pathology through different mechanisms. Oligomeric forms alter the conformation paired helical filament-like manner. This effect occurs without hyperphosphorylation as well activation specific kinases, suggesting induce assembly nucleation effect. Monomers, turn, neurodegeneration calpain-mediated cleavage leads to...
During the last decade, much progress has been made in developing protocols for differentiation of human embryonic stem cells (hESCs) into a neural phenotype. The appropriate agent cell therapy is precursors (NPs). Here, we demonstrate derivation highly enriched and expandable populations proliferating NPs from CCTL14 line hESCs. These could differentiate vitro functionally active neurons, as confirmed by immunohistochemical staining electrophysiological analysis. Neural differentiated hESCs...
Abstract Muscle‐specific kinase myasthenia gravis (MuSK MG) is caused by autoantibodies against MuSK in the neuromuscular junction (NMJ). MG patients have fluctuating, fatigable skeletal muscle weakness, particular of bulbar muscles. Severity differs greatly between patients, spite comparable autoantibody levels. One explanation for inter‐patient and inter‐muscle variability sensitivity might be variations compensatory responses. Previously, we developed a passive transfer mouse model MG. In...
Current efforts to improve muscle performance are focused on trophism via inhibition of the myostatin pathway: however they have been unsuccessful in clinic date. In this study, a novel protein has created by combining soluble activin receptor, strong inhibitor, C-terminal agrin nLG3 domain (ActR-Fc-nLG3) involved development and maintenance neuromuscular junctions. Both domains connected constant region an Igg1 monoclonal antibody. Surprisingly, young male mice treated with ActR-Fc-nLG3...
Muscle-specific kinase myasthenia gravis (MuSK MG) is caused by autoantibodies against MuSK in the neuromuscular junction (NMJ). MG patients have fluctuating, fatigable weakness, particular of bulbar muscles. Severity differs greatly between patients, spite comparable autoantibody levels. One explanation for inter-patient and inter-muscle variability sensitivity might be variations compensatory muscle responses. Previously, we developed a passive transfer mouse model MG. In preliminary ex...