Vascular endothelial growth factor C [Neurosurgery Wiki]

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====== Vascular endothelial growth factor C ======

Emergence of dysmorphic [[neuron]]s is the primary [[pathology]] in [[focal cortical dysplasia]] (FCD) associated pediatric [[intractable epilepsy]]; however, the etiologies related to the development and function of dysmorphic neurons are not fully understood. 

Previous studies revealed that the expression of [[vascular endothelial growth factor]]-C (VEGF-C) and corresponding receptors VEGFR-2, VEGFR-3 was increased in the epileptic lesions of patients with [[tuberous sclerosis complex]] or [[mesial temporal lobe epilepsy]]. 

Shen etal. showed that the expression of VEGF-C, VEGFR-2, and VEGFR-3 was increased at both [[mRNA]] and protein levels in patients with cortical lesions of type I, IIa, and IIb FCD. The immunoreactivity of VEGF-C, VEGFR-2 and VEGFR-3 was located in the micro-columnar neurons in FCD type I lesions, dysplastic neurons (DNs) in FCD type IIa lesions, balloon cells (BCs) and astrocytes in FCD type IIb lesions. Additionally, the amplitude of evoked-EPSCs (eEPSC) mediated by NMDA receptor, the ratio of NMDA receptor- and AMPA receptor-mediated eEPSC were increased in the dysmorphic neurons of FCD rats established by prenatal X-ray radiation. Furthermore, NMDA receptor mediated current in dysmorphic neurons was further potentiated by exogenous administration of VEGF-C, however, could be antagonized by ki8751, the blocker of VEGFR-2. These results suggest that VEGF-C system participate in the pathogenesis of cortical lesions in patients with FCD in association with modulating NMDA receptor-mediated currents
((Shen KF, Duan QT, Duan W, Xu SL, An N, Ke YY, Wang LT, Liu SY, Yang H, Zhang CQ. [[Vascular endothelial growth factor]]-C modulates cortical NMDA receptor activity in cortical lesions of young patients and rat model with [[focal cortical dysplasia]]. Brain Pathol. 2022 Mar 8:e13065. doi: 10.1111/bpa.13065. Epub ahead of print. PMID: 35259773.)).