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LINC00894 Regulates Cerebral Ischemia/Reperfusion Injury by Stabilizing EIF5 and Facilitating ATF4-Mediated Induction of FGF21 and ACOD1 Expression.
Chen, Yifei; Cui, Hengxiang; Han, Zhuanzhuan; Xu, Lei; Wang, Lin; Zhang, Yuefei; Liu, Lijun.
Afiliación
  • Chen Y; Department of Emergency and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, No.1055, San Xiang Road, Suzhou, Jiangsu, 215004, China.
  • Cui H; Department of Emergency Medicine, The Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, 225012, China.
  • Han Z; Shanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, Shanghai Mental Health Center, National Center for Mental Disorders, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
  • Xu L; Department of Emergency Medicine, The Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, 225012, China.
  • Wang L; Department of Emergency Medicine, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China.
  • Zhang Y; Department of Anesthesiology, The Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, 225012, China.
  • Liu L; Department of Emergency Medicine, The Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, 225012, China.
Neurochem Res ; 49(10): 2910-2925, 2024 Oct.
Article en En | MEDLINE | ID: mdl-39060766
ABSTRACT
The non-coding RNA LINC00894 modulates tumor proliferation and drug resistance. However, its role in brain is still unclear. Using RNA-pull down combined with mass spectrometry and RNA binding protein immunoprecipitation, EIF5 was identified to interact with LINC00894. Furthermore, LINC00894 knockdown decreased EIF5 protein expression, whereas LINC00894 overexpression increased EIF5 protein expression in SH-SY5Y and BE(2)-M17 (M17) neuroblastoma cells. Additionally, LINC00894 affected the ubiquitination modification of EIF5. Adeno-associated virus (AAV) mediated LINC00894 overexpression in the brain inhibited the expression of activated Caspase-3, while increased EIF5 protein level in rats and mice subjected to transient middle cerebral artery occlusion reperfusion (MCAO/R). Meanwhile, LINC00894 knockdown increased the number of apoptotic cells and expression of activated Caspase-3, and its overexpression decreased them in the oxygen-glucose deprivation and reoxygenation (OGD/R) in vitro models. Further, LINC00894 was revealed to regulated ATF4 protein expression in condition of OGD/R and normoxia. LINC00894 knockdown also decreased the expression of glutamate-cysteine ligase catalytic subunit (GCLC) and ATF4, downregulated glutathione (GSH), and the ratio of GSH to oxidized GSH (GSH GSSG) in vitro. By using RNA-seq combined with qRT-PCR and immunoblot, we identified that fibroblast growth factor 21 (FGF21) and aconitate decarboxylase 1 (ACOD1), as the ATF4 target genes were regulated by LINC00894 in the MCAO/R model. Finally, we revealed that ATF4 transcriptionally regulated FGF21 and ACOD1 expression; ectopic overexpression of FGF21 or ACOD1 in LINC00894 knockdown cells decreased activated Caspase-3 expression in the OGD/R model. Our results demonstrated that LINC00894 regulated cerebral ischemia injury by stabilizing EIF5 and facilitating EIF5-ATF4-dependent induction of FGF21 and ACOD1.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Factor de Transcripción Activador 4 / Factores de Crecimiento de Fibroblastos / ARN Largo no Codificante Límite: Animals / Humans / Male Idioma: En Revista: Neurochem Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Factor de Transcripción Activador 4 / Factores de Crecimiento de Fibroblastos / ARN Largo no Codificante Límite: Animals / Humans / Male Idioma: En Revista: Neurochem Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos