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Increasing expression of dual-specificity phosphatase 12 mitigates oxygen-glucose deprivation/reoxygenation-induced neuronal apoptosis and inflammation through inactivation of the ASK1-JNK/p38 MAPK pathway.
He, Jiaxuan; Li, Siyuan; Teng, Yunpeng; Xiong, Hongfei; Wang, Zhuang; Han, Xiaoyao; Gong, Wei; Gao, Ya.
Afiliación
  • He J; Anesthesia & Comfort Medical Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi Province, China.
  • Li S; Department of Pediatric Surgery, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
  • Teng Y; Anesthesia & Comfort Medical Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi Province, China.
  • Xiong H; Anesthesia & Comfort Medical Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi Province, China.
  • Wang Z; Anesthesia & Comfort Medical Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi Province, China.
  • Han X; Anesthesia & Comfort Medical Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi Province, China.
  • Gong W; Anesthesia & Comfort Medical Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi Province, China.
  • Gao Y; Department of Pediatric Surgery, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Autoimmunity ; 57(1): 2345919, 2024 Apr 22.
Article en En | MEDLINE | ID: mdl-38721693
ABSTRACT
Dual-specificity phosphatase 12 (DUSP12) is abnormally expressed under various pathological conditions and plays a crucial role in the pathological progression of disorders. However, the role of DUSP12 in cerebral ischaemia/reperfusion injury has not yet been investigated. This study explored the possible link between DUSP12 and cerebral ischaemia/reperfusion injury using an oxygen-glucose deprivation/reoxygenation (OGD/R) model. Marked decreases in DUSP12 levels have been observed in cultured neurons exposed to OGD/R. DUSP12-overexpressed neurons were resistant to OGD/R-induced apoptosis and inflammation, whereas DUSP12-deficient neurons were vulnerable to OGD/R-evoked injuries. Further investigation revealed that DUSP12 overexpression or deficiency affects the phosphorylation of apoptosis signal-regulating kinase 1 (ASK1), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) in neurons under OGD/R conditions. Moreover, blockade of ASK1 diminished the regulatory effect of DUSP12 deficiency on JNK and p38 MAPK activation. In addition, DUSP12-deficiency-elicited effects exacerbating neuronal OGD/R injury were reversed by ASK1 blockade. In summary, DUSP12 protects against neuronal OGD/R injury by reducing apoptosis and inflammation through inactivation of the ASK1-JNK/p38 MAPK pathway. These findings imply a neuroprotective function for DUSP12 in cerebral ischaemia/reperfusion injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxígeno / Daño por Reperfusión / Apoptosis / MAP Quinasa Quinasa Quinasa 5 / Proteínas Quinasas p38 Activadas por Mitógenos / Fosfatasas de Especificidad Dual / Glucosa / Inflamación / Neuronas Límite: Animals Idioma: En Revista: Autoimmunity Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxígeno / Daño por Reperfusión / Apoptosis / MAP Quinasa Quinasa Quinasa 5 / Proteínas Quinasas p38 Activadas por Mitógenos / Fosfatasas de Especificidad Dual / Glucosa / Inflamación / Neuronas Límite: Animals Idioma: En Revista: Autoimmunity Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido