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CYR61 is Involved in Neonatal Hypoxic-ischemic Brain Damage Via Modulating Astrocyte-mediated Neuroinflammation.
Jin, Dongmei; Dai, Zhushan; Zhao, Lili; Ma, Tongyao; Ma, Yanru; Zhang, Zhongxu.
Afiliación
  • Jin D; Department of Neonatology, the First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China. Electronic address: 600440@hrbmu.edu.cn.
  • Dai Z; Department of Neonatology, the First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
  • Zhao L; Department of Neonatology, the First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
  • Ma T; Department of Neonatology, the First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
  • Ma Y; Department of Neonatology, the First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
  • Zhang Z; Department of Oncology, the First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Neuroscience ; 552: 54-64, 2024 Aug 06.
Article en En | MEDLINE | ID: mdl-38908506
ABSTRACT
The activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome in astrocytes has been found in the hypoxic-ischemic brain damage (HIBD) model. Cysteine rich angiogenic inducer 61 (CYR61) is secreted by reactive astrocytes. However, the effects of CYR61 on HIBD and its related mechanisms remain unclear. This study sought to explore the role of CYR61 in the activation of astrocytes and the NLRP3 inflammasome in neonatal HIBD. HIBD models were established in 7-day Sprague-Dawley rat pups. Neurobehavioral evaluation and 2,3,5-triphenyl-tetrazolium chloride staining were performed. In addition, rat primary astrocytes were used to establish the cell model of HIBD in vitro by oxygen-glucose deprivation/reperfusion (OGD/R). Then, CYR61-overexpression and sh-CYR61 viruses mediated by lentivirus were transduced into ODG/R-treated primary astrocytes. The expressions of related genes were evaluated using real-time quantitative PCR, western blot, immunofluorescence staining, and Enzyme-linked immunosorbent assay. The results showed that hypoxia-ischemia induced short-term neurological deficits, neuronal damage, and cerebral infarction in neonatal rats. In vivo, the expressions of CYR61, NLRP3, and glial fibrillary acidic protein (GFAP) were up-regulated in the HIBD model. In vitro, CYR61 exhibited high expression. CYR61 overexpression increased the expressions of GFAP and C3, whereas decreased S100A10 expression. CYR61 overexpression increased the expression of NLRP3, ASC, caspase-1 p20 and IL-1ß. CYR61 overexpression activated NF-κB by promoting the phosphorylation of IκBα and p65. Thus, CYR61 is involved in neonatal HIBD progress, which may be related to the activation of astrocytes, the NLRP3 inflammasome, and the NF-κB signaling pathway.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Astrocitos / Ratas Sprague-Dawley / Hipoxia-Isquemia Encefálica / Proteína 61 Rica en Cisteína / Proteína con Dominio Pirina 3 de la Familia NLR / Animales Recién Nacidos Límite: Animals Idioma: En Revista: Neuroscience Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Astrocitos / Ratas Sprague-Dawley / Hipoxia-Isquemia Encefálica / Proteína 61 Rica en Cisteína / Proteína con Dominio Pirina 3 de la Familia NLR / Animales Recién Nacidos Límite: Animals Idioma: En Revista: Neuroscience Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos