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Protective effect of DLX6-AS1 silencing against cerebral ischemia/reperfusion induced impairments.
Hu, Xiamin; Xiang, Zifei; Zhang, Wei; Yu, Zhijun; Xin, Xiaoming; Zhang, Rong; Deng, Youping; Yuan, Qiong.
Afiliación
  • Hu X; College of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai, China.
  • Xiang Z; Institute of Pharmaceutical Innovation, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, College of Medicine, Wuhan University of Science and Technology, Wuhan, Hubei Province, China.
  • Zhang W; China Resources and WISCO General Hospital, Wuhan, Hubei Province, China.
  • Yu Z; Institute of Pharmaceutical Innovation, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, College of Medicine, Wuhan University of Science and Technology, Wuhan, Hubei Province, China.
  • Xin X; College of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai, China.
  • Zhang R; Institute of Pharmaceutical Innovation, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, College of Medicine, Wuhan University of Science and Technology, Wuhan, Hubei Province, China.
  • Deng Y; Bioinformatics Core, Department of Complementary and Integrative Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, HI 96813, USA.
  • Yuan Q; Institute of Pharmaceutical Innovation, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, College of Medicine, Wuhan University of Science and Technology, Wuhan, Hubei Province, China.
Aging (Albany NY) ; 12(22): 23096-23113, 2020 11 18.
Article en En | MEDLINE | ID: mdl-33216728
ABSTRACT
In the present study, we investigated the role of lncRNA mus distal-less homeobox 6 antisense 1 (DLX6-AS1) during cerebral impairment induced by stroke. DLX6-AS1 levels were upregulated during ischemia/reperfusion (I/R) and downregulation of DLX6-AS1 reduced acute injury and ameliorated long-term neurological impairments induced by cerebral I/R in mice. Additionally, silencing of DLX6-AS1 significantly decreased the neuronal apoptosis in vivo and in vitro. Furthermore, inhibition of miRNA-149-3p led to enhance the apoptosis, which confirmed that DLX6-AS1 could sponge miR-149-3p. Finally, BOK was predicted to be the target of miR-149-3p using TargetScanVert software. And the silencing of DLX6-AS1 inhibited BOK expression both in vivo and in vitro, which was reversed by a miR-149-3p inhibitor. At meantime, BOK promoted OGD/R induced apoptosis in N2a cells. Therefore, this suggests that miR-149-3p sponging by DLX6-AS1 may lead to cerebral neuron I/R-induced impairments through upregulation of apoptotic BOK activity, which offers a new approach to the treatment of stroke impairment.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Conducta Animal / Daño por Reperfusión / Infarto de la Arteria Cerebral Media / Interferencia de ARN / ARN Largo no Codificante / Tratamiento con ARN de Interferencia / Neuronas Límite: Animals / Humans / Male Idioma: En Revista: Aging (Albany NY) Asunto de la revista: GERIATRIA Año: 2020 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Conducta Animal / Daño por Reperfusión / Infarto de la Arteria Cerebral Media / Interferencia de ARN / ARN Largo no Codificante / Tratamiento con ARN de Interferencia / Neuronas Límite: Animals / Humans / Male Idioma: En Revista: Aging (Albany NY) Asunto de la revista: GERIATRIA Año: 2020 Tipo del documento: Article País de afiliación: China