ArticlePloS one2016
Inhibition of Vascular Endothelial Growth Factor Receptor 2 Exacerbates Loss of Lower Motor Neurons and Axons during Experimental Autoimmune Encephalomyelitis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- RTMS Mitigates Simulated Spaceflight-Induced Emotional Dysfunction Through VEGFR-2-Mediated Neuroprotection.Brain and behavior · 2026Article
- Integrated elemental analysis supports targeting copper perturbations as a therapeutic strategy in multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Tyrosine kinases: multifaceted receptors at the intersection of several neurodegenerative disease-associated processes.Frontiers in dementia · 2024Review
- Histamine H4 Receptor Agonist, 4-Methylhistamine, Aggravates Disease Progression and Promotes Pro-Inflammatory Signaling in B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model.International journal of molecular sciences · 2023Article
- The UPR Maintains Proteostasis and the Viability and Function of Hippocampal Neurons in Adult Mice.International journal of molecular sciences · 2023Article
- Integrated Analysis and Identification of CSF-Derived Risk miRNAs and Pivotal Genes in Multiple Sclerosis.Journal of molecular neuroscience : MN · 2022Article
- Chronic experimental autoimmune encephalomyelitis is an excellent model to study neuroaxonal degeneration in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Article
- Effect and Mechanism of Catalpol on Remyelination via Regulation of the NOTCH1 Signaling Pathway.Frontiers in pharmacology · 2021Article
- miR-129-5p and miR-130a-3p Regulate VEGFR-2 Expression in Sensory and Motor Neurons during Development.International journal of molecular sciences · 2020Article
- Liver kinase B1 depletion from astrocytes worsens disease in a mouse model of multiple sclerosis.Glia · 2020Article
- Oligodendrocyte-specific ATF4 inactivation does not influence the development of EAE.Journal of neuroinflammation · 2019Article
- Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis.Neural regeneration research · 2018Review
- Neuroprotective effects of vascular endothelial growth factor A in the experimental autoimmune encephalomyelitis model of multiple sclerosis.Neural regeneration research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are inflammatory demyelinating and neurodegenerative diseases in the central nervous system (CNS). It is believed that MS and EAE are initiated by autoreactive T lymphocytes that recognize myelin antigens; however, the mechanisms responsible for neurodegeneration in these diseases remain elusive. Data indicate that vascular endothelial growth factor A (VEGF-A) plays a role in the development of MS and EAE. Interestingly, VEGF-A is regarded as a neurotrophic factor in the CNS that promotes neuron survival and neurogenesis in various neurodegenerative diseases by activating VEGF receptor 2 (VEGFR2). In this study, we sought to explore the role of the VEGF-A/VEGFR2 signaling in neurodegeneration in MS and EAE. We showed that the expression of VEGF-A was decreased in the spinal cord during EAE and that VEGFR2 was activated in lower motor neurons in the spinal cord of EAE mice. Interestingly, we found that treatment with SU5416, a selective VEGFR2 inhibitor, starting after the onset of EAE clinical symptoms exacerbated lower motor neuron loss and axon loss in the lumbar spinal cord of mice undergoing EAE, but did not alter Purkinje neuron loss in the cerebellum or upper motor neuron loss in the cerebral cortex. Moreover, SU5416 treatment had a minimal effect on EAE clinical symptoms as well as inflammation, demyelination, and oligodendrocyte loss in the lumbar spinal cord. These results imply the protective effects of the VEGF-A/VEGFR2 signaling on lower motor neurons and axons in the spinal cord in MS and EAE.
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