Emmanuel Hermans

ORCID: 0000-0002-8589-3279
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Receptor Mechanisms and Signaling
  • Neuropeptides and Animal Physiology
  • Neurotransmitter Receptor Influence on Behavior
  • Pain Mechanisms and Treatments
  • Amyotrophic Lateral Sclerosis Research
  • Cannabis and Cannabinoid Research
  • Amino Acid Enzymes and Metabolism
  • Neurogenesis and neuroplasticity mechanisms
  • Nerve injury and regeneration
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Ion channel regulation and function
  • Neurogenetic and Muscular Disorders Research
  • Parkinson's Disease Mechanisms and Treatments
  • Pharmacological Effects and Assays
  • Pharmacological Receptor Mechanisms and Effects
  • Chemical Synthesis and Analysis
  • Pancreatic function and diabetes
  • Hypothalamic control of reproductive hormones
  • Protein Kinase Regulation and GTPase Signaling
  • Nicotinic Acetylcholine Receptors Study
  • Spinal Cord Injury Research
  • Mesenchymal stem cell research
  • GABA and Rice Research
  • Neurological disorders and treatments

UCLouvain
2016-2025

Ghent University
2023

Ghent University Hospital
2023

Herman Miller (United States)
2007

de Duve Institute
2005

Physiol (Belgium)
2005

University of Leicester
1998-2000

KU Leuven
1997

We outline a powerful method for the directed evolution of integral membrane proteins in inner Escherichia coli . For mammalian G protein-coupled receptor, we arrived at sequence with an order-of-magnitude increase functional expression that still retains biochemical properties wild type. This mutant also shows enhanced heterologous eukaryotes (12-fold Pichia pastoris and 3-fold HEK293T cells) greater stability when solubilized purified, indicating biophysical protein had been under pressure...

10.1073/pnas.0803103105 article EN Proceedings of the National Academy of Sciences 2008-09-24

Abstract Adult mesenchymal stem cells (MSCs) exhibit neuroprotective properties when introduced into the degenerating central nervous system through different putative mechanisms including secretion of growth factors and transdifferentiation. In present study, we injected MSCs cerebrospinal fluid symptomatic hSOD1 G93A rats, a transgenic animal model familial amyotrophic lateral sclerosis (ALS) expressing mutated form human superoxide dismutase. were found to infiltrate parenchyma migrate...

10.1002/jnr.22038 article EN Journal of Neuroscience Research 2009-03-06

Type-1 cannabinoid (CB1) and leptin (ObR) receptors regulate metabolic astroglial functions, but the potential links between two systems in astrocytes were not investigated so far. Genetic pharmacological manipulations of CB1 receptor expression activity cultured cortical hypothalamic demonstrated that signaling controls levels ObR expression. Lack also markedly impaired leptin-mediated activation signal transducers activators transcription 3 5 (STAT3 STAT5) astrocytes. In particular,...

10.1016/j.molmet.2013.08.001 article EN cc-by-nc-sa Molecular Metabolism 2013-08-09

Abstract Excitatory transmission in the CNS necessitates existence of dynamic controls glutamate uptake achieved by astrocytes, both physiological conditions and under pathological circumstances characterized gliosis. In this context, study was aimed at evaluating involvement group I metabotropic receptors (mGluR) regulation transport a model rat astrocytes undergoing vitro activation using cocktail growth factors (G5 supplement). The vast majority cells were found to take up aspartate,...

10.1111/j.1471-4159.2005.03216.x article EN Journal of Neurochemistry 2005-06-10

Abstract Pharmacological effects of amantadine on dopaminergic transmission are proposed to result from an uncompetitive antagonism at glutamate N ‐methyl‐ d ‐aspartate (NMDA) receptors. However, our previous studies examining amantadine‐mediated dopamine receptor regulation in the rat striatum revealed a discrepancy direct interference with transmission. Preliminary vitro binding data literature suggested interaction sigma 1 receptor. Therefore, we have now further characterized...

10.1111/j.0953-816x.2004.03297.x article EN European Journal of Neuroscience 2004-04-01

There is considerable evidence that the activity of neuronal dopamine transporter (DAT) dynamically regulated and a putative implication its phosphorylation in this process has been proposed. However, there little information available regarding nature physiological stimuli contribute to endogenous control DAT function. Based on close relationship between glutamatergic dopaminergic systems striatum, we investigated modulation by metabotropic glutamate receptors (mGluRs). Short‐term...

10.1046/j.1471-4159.2001.00179.x article EN Journal of Neurochemistry 2001-03-01

Abstract While the astrocytic control of extracellular glutamate concentration at synaptic contacts is well characterized, little known regarding clearance along axon tracts, even though local excitotoxic damage has been reported. Therefore, we have compared handling in astrocyte cultures derived from white matter (corpus callosum) and grey tissues (cortical structures). These populations astrocytes showed clearly distinct phenotypes, adopting stellate or protoplasmic morphologies...

10.1111/j.1471-4159.2009.05889.x article EN Journal of Neurochemistry 2009-02-13

Peroxiredoxin-5 (PRDX5) is an antioxidant enzyme which differs from the other peroxiredoxins with regards to its enzymatic mechanism, high affinity for organic peroxides and peroxynitrite wide subcellular distribution. In particular, mitochondrial isoform of PRDX5 confers a remarkable cytoprotection toward oxidative stress mammalian cells. Mitochondrial dysfunction disruption Ca²⁺ homeostasis are implicated in neurodegeneration. Growing evidence supports that endoplasmic reticulum (ER) could...

10.1111/jnc.12117 article EN Journal of Neurochemistry 2012-12-06

Abstract Background Neuroinflammation and nitroxidative stress are implicated in the pathophysiology of neuropathic pain. In view both processes, microglial astroglial activation spinal dorsal horn play a predominant role. The present study investigated severity pain degree glial an inflammatory- nitroxidative-prone animal model. Methods Transgenic rats expressing mutated superoxide dismutase 1 (hSOD1 G93A ) classically used as model for amyotrophic lateral sclerosis (ALS). Because...

10.1186/1742-2094-8-33 article EN cc-by Journal of Neuroinflammation 2011-04-13

Multipotent mesenchymal stem (stromal) cells (MSCs) have been credited with immunomodulative properties, supporting beneficial outcomes when transplanted into a variety of disease models involving inflammation. Potential mechanisms include the secretion paracrine factors and establishment neurotrophic microenvironment. To test hypothesis that MSCs release soluble mediators can attenuate local inflammation, we here analysed influence on activation microglia cells, as well inflammatory...

10.1186/s12974-014-0157-8 article EN cc-by Journal of Neuroinflammation 2014-09-11

Abstract The astrocytic cystine/glutamate antiporter system x c − represents an important source of extracellular glutamate in the central nervous system, with potential impact on excitatory neurotransmission. Yet, its function and importance brain physiology remain incompletely understood. Employing slice electrophysiology mice a genetic deletion specific subunit , xCT (xCT −/− mice), we uncovered decreased neurotransmission at corticostriatal synapses. This effect was partly mitigated by...

10.1038/s41380-020-0751-3 article EN cc-by Molecular Psychiatry 2020-05-04

Abstract Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective loss of motor neurones accompanied intense gliosis in lesioned areas the brain and spinal cord. Glutamate‐mediated excitotoxicity resulting from impaired astroglial uptake constitutes one current pathophysiological hypotheses explaining progression disease. In this study, we examined regulation glutamate transporters type 5 metabotropic receptor (mGluR5) activated astrocytes derived...

10.1111/j.1471-4159.2005.03577.x article EN Journal of Neurochemistry 2005-12-20
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