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Doctoral Thesis
DOI
https://doi.org/10.11606/T.42.2018.tde-05022018-171917
Document
Author
Full name
Wesley Nogueira Brandão
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2017
Supervisor
Committee
Peron, Jean Pierre Schatzmann (President)
Almeida, Rafael Ribeiro
Keller, Alexandre de Castro
Munhoz, Carolina Demarchi
Vieira, Pedro Manoel Mendes de Moraes
Title in Portuguese
Glutamato através da sinalização pelo NMDAR modula a resposta inata de células imunitárias in vitro durante hipóxia.
Keywords in Portuguese
Acidente vascular cerebral
Células da microglia
Glutamato
Hipóxia
NMDAr
Abstract in Portuguese
O Acidente vascular cerebral é uma doença aguda neuroinflamatória cuja prevalência aumentou nos últimos anos. Seus sintomas são decorrente da morte neuronal provocada pela privação de glicose e oxigênio. Após a morte neuronal, há liberação de citocinas, radicais livres e neurotransmissores, dentre eles o glutamato. Nosso objetivo é averiguar como o glutamato através do seu receptor NMDA modula a resposta inflamatória tanto de células residentes do SNC, quanto de células imunes infiltrantes. Para a realização desse estudos, realizamos experimentos in vitro e in vivo com o bloqueador do NMDAr, sob o processo de hipóxia. Nossos resultados demonstraram que a sinalização por NMDAr modula a expressão de moléculas envolvidas na apresentação de antígeno em células da microglia e macrófagos, bem como na produção de óxido nítrico por neutrófilos. O seu bloqueio diminui morte celular e lesão cerebral. Por fim, nossa pesquisa mostra que a sinalização NMDAr está envolvido não só com excitotoxicidade, mas também com a modulação da resposta da células inata.
Title in English
Glutamate through NMDAr signaling modulates the immune cell response in vitro during hypoxia.
Keywords in English
Cerebral vascular accident
Glutamate
Hypoxia
Microglia cells
NMDAr
Abstract in English
Stroke is an acute neuroinflammatory disease whose prevalence has increased in recent years. Its symptoms are due to the neuronal death caused by the deprivation of glucose and oxygen. After neuronal death, there is release of cytokines, free radicals and neurotransmitters, among them glutamate. Our goal is to investigate how glutamate through its NMDA receptor modulates the inflammatory response of both resident CNS cells and infiltrating immune cells. For the accomplishment of these studies, we performed experiments in vitro and in vivo with the NMDAr blocker under the hypoxia process. Our results demonstrated that NMDAr signaling modulates the expression of molecules involved in the presentation of antigen in microglia and macrophages cells, as well as in the production of nitric oxide by neutrophils. Its blockage decreases cell death and brain damage. Finally, our research shows that NMDAr signaling is involved not only with excitotoxicity, but also with the modulation of the innate cell response.
 
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Release Date
2020-02-05
Publishing Date
2018-02-05
 
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