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Altered expression of the Plexin-B2 system in tuberous sclerosis complex and focal cortical dysplasia IIb lesions

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dc.contributor.authorDai, Lu
dc.contributor.authorHuang, Jun
dc.contributor.authorShen, Kai-Feng
dc.contributor.authorYang, Xiao-lin
dc.contributor.authorZhu, Gang
dc.contributor.authorZhang, Li
dc.contributor.authorWang, Zhong-ke
dc.contributor.authorLiu, Shi-yong
dc.contributor.authorLiao, Xiang
dc.contributor.authorXu, Sen-lin
dc.contributor.authorYang, Hui
dc.contributor.authorLi, Xing-yi
dc.contributor.authorZhang, Chun-Qing
dc.date.accessioned2024-09-09T08:28:24Z
dc.date.available2024-09-09T08:28:24Z
dc.date.issued2024
dc.description.abstractTuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD) type IIb are the predominant causes of drug-refractory epilepsy in children. Dysmorphic neurons (DNs), giant cells (GCs), and balloon cells (BCs) are the most typical pathogenic profiles in cortical lesions of TSC and FCD IIb patients. However, mechanisms underlying the pathological processes of TSC and FCD IIb remain obscure. The Plexin-B2-Sema4C signalling pathway plays critical roles in neuronal morphogenesis and corticogenesis during the development of the central nervous system. However, the role of the Plexin-B2 system in the pathogenic process of TSC and FCD IIb has not been identified. In the present study, we investigated the expression and cell distribution characteristics of Plexin-B2 and Sema4C in TSC and FCD IIb lesions with molecular technologies. Our results showed that the mRNA and protein levels of Plexin-B2 expression were significantly increased both in TSC and FCD IIb lesions versus that in the control cortex. Notably, Plexin-B2 was also predominantly observed in GCs in TSC epileptic lesions and BCs in FCD IIb lesions. In contrast, the expression of Sema4C, the ligand of Plexin-B2, was significantly decreased in DNs, GCs, and BCs in TSC and FCD IIb epileptic lesions. Additionally, Plexin-B2 and Sema4C were expressed in astrocytes and microglia cells in TSC and FCD IIb lesions. Furthermore, the expression of Plexin-B2 was positively correlated with seizure frequency in TSC and FCD IIb patients. In conclusion, our results showed the Plexin-B2-Sema4C system was abnormally expressed in cortical lesions of TSC and FCD IIb patients, signifying that the Plexin-B2-Sema4C system may play a role in the pathogenic development of TSC and FCD IIb.es
dc.formatapplication/pdfes
dc.format.extent17es
dc.identifier.doihttps://doi.org/10.14670/HH-18-707
dc.identifier.eisbnHistology and Histopathology Vol. 39, nº9 (2024)es
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/143724
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectEpilepsyes
dc.subjectMalformation of cortical developmentes
dc.subjectPlexin-B2es
dc.subjectSema4Ces
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleAltered expression of the Plexin-B2 system in tuberous sclerosis complex and focal cortical dysplasia IIb lesionses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.39, nº9 (2024)