ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2019
Increased expression of vascular endothelial growth factor-C and vascular endothelial growth factor receptor-3 after pilocarpine-induced status epilepticus in mice.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 17 citations in OpenAlex.
- Reply to: Letter to the Editor - Extending the Phase-dependent VEGF Framework to Post-Intracerebral Hemorrhage Epileptogenesis.Revista de neurologia · 2026Article
- Beyond Neurovascular Repair: Should Epileptogenesis Inform VEGF Therapy After Intracerebral Hemorrhage?Revista de neurologia · 2026Article
- Astrocytes in Genetic Epilepsies: Supporting Actor or Key Player?Journal of neuroscience research · 2026Review
- The Role of Blood-Brain Barrier Disruption in Epilepsy: Mechanisms and Consequences.Neurology international · 2025Review
- Beyond vessels: unraveling the impact of VEGFs on neuronal functions and structure.Journal of biomedical science · 2025Review
- VEGFR-3 signaling in macrophages: friend or foe in disease?Frontiers in immunology · 2024Review
- Eugenol alleviates neuronal damage via inhibiting inflammatory process against pilocarpine-induced status epilepticus.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Alleviation of hippocampal necroptosis and neuroinflammation by NecroX-7 treatment after acute seizures.Frontiers in pharmacology · 2023Article
- Overview of the meningeal lymphatic vessels in aging and central nervous system disorders.Cell & bioscience · 2022Review
- Changes of biochemical biomarkers in the serum of children with convulsion status epilepticus: a prospective study.BMC neurology · 2022Article
- Interleukin-17A Mediates Hippocampal Damage and Aberrant Neurogenesis Contributing to Epilepsy-Associated Anxiety.Frontiers in molecular neuroscience · 2022Article
- lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Astrocyte Role in Temporal Lobe Epilepsy and Development of Mossy Fiber Sprouting.Frontiers in cellular neuroscience · 2021Review
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5 authors at 1 institution in 1 country.
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Abstract
Vascular endothelial growth factor (VEGF)-C and its receptor, vascular endothelial growth factor receptor (VEGFR)-3, are responsible for lymphangiogenesis in both embryos and adults. In epilepsy, the expression of VEGF-C and VEGFR-3 was significantly upregulated in the human brains affected with temporal lobe epilepsy. Moreover, pharmacologic inhibition of VEGF receptors after acute seizures could suppress the generation of spontaneous recurrent seizures, suggesting a critical role of VEGF-related signaling in epilepsy. Therefore, in the present study, the spatiotemporal expression of VEGF-C and VEGFR-3 against pilocarpine-induced status epilepticus (SE) was investigated in C57BL/6N mice using immunohistochemistry. At 1 day after SE, hippocampal astrocytes and microglia were activated. Pyramidal neuronal death was observed at 4 days after SE. In the subpyramidal zone, VEGF-C expression gradually increased and peaked at 7 days after SE, while VEGFR-3 was significantly upregulated at 4 days after SE and began to decrease at 7 days after SE. Most VEGF-C/VEGFR-3-expressing cells were pyramidal neurons, but VEGF-C was also observed in some astrocytes in sham-manipulated animals. However, at 4 days and 7 days after SE, both VEGFR-3 and VEGF-C immunoreactivities were observed mainly in astrocytes and in some microglia of the stratum radiatum and lacunosum-moleculare of the hippocampus, respectively. These data indicate that VEGF-C and VEGFR-3 can be upregulated in hippocampal astrocytes and microglia after pilocarpine-induced SE, providing basic information about VEGF-C and VEGFR-3 expression patterns following acute seizures.
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