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Blood-brain barrier disruption and angiogenesis in a rat model for neurocysticercosis

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dc.contributor.author Carmen-Orozco, Rogger P.
dc.contributor.author Dávila-Villacorta, Danitza G.
dc.contributor.author Cauna, Yudith
dc.contributor.author Bernal-Teran, Edson G.
dc.contributor.author Bitterfeld, Leandra
dc.contributor.author Sutherland, Graham L.
dc.contributor.author Chile, Nancy
dc.contributor.author Céliz, Rensson H.
dc.contributor.author Ferrufino-Schmidt, María C.
dc.contributor.author Gavídia, Cesar M.
dc.contributor.author Sterling, Charles R.
dc.contributor.author García, Héctor H.
dc.contributor.author Gilman, Robert H.
dc.contributor.author Verástegui, Manuela Renee
dc.date.accessioned 2018-11-30T02:09:30Z
dc.date.available 2018-11-30T02:09:30Z
dc.date.issued 2018
dc.identifier.uri https://hdl.handle.net/20.500.12866/4016
dc.description.abstract Neurocysticercosis (NCC) is a helminth infection affecting the central nervous system caused by the larval stage (cysticercus) of Taenia solium. Since vascular alteration and blood-brain barrier (BBB) disruption contribute to NCC pathology, it is postulated that angiogenesis could contribute to the pathology of this disease. This study used a rat model for NCC and evaluated the expression of two angiogenic factors called vascular endothelial growth factor (VEGF-A) and fibroblast growth factor (FGF2). Also, two markers for BBB disruption, the endothelial barrier antigen and immunoglobulin G, were evaluated using immunohistochemical and immunofluorescence techniques. Brain vasculature changes, BBB disruption, and overexpression of angiogenesis markers surrounding viable cysts were observed. Both VEGF-A and FGF2 were overexpressed in the tissue surrounding the cysticerci, and VEGF-A was overexpressed in astrocytes. Vessels showed decreased immunoreactivity to endothelial barrier antigen marker and an extensive staining for IgG was found in the tissues surrounding the cysts. Additionally, an endothelial cell tube formation assay using human umbilical vein endothelial cells showed that excretory and secretory antigens of T. solium cysticerci induce the formation of these tubes. This in vitro model supports the hypothesis that angiogenesis in NCC might be caused by the parasite itself, as opposed to the host inflammatory responses alone. In conclusion, brain vasculature changes, BBB disruption, and overexpression of angiogenesis markers surrounding viable cysts were observed. This study also demonstrates that cysticerci excretory-secretory processes alone can stimulate angiogenesis. en_US
dc.language.iso eng
dc.publisher Wiley
dc.relation.ispartof urn:issn:1097-4547
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject angiogenesis en_US
dc.subject BBB disruption en_US
dc.subject neurocysticercosis en_US
dc.subject T. solium en_US
dc.subject VEGF-A en_US
dc.title Blood-brain barrier disruption and angiogenesis in a rat model for neurocysticercosis en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1002/jnr.24335
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.00 es_PE
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.01.04


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