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lncRNA PRR34-AS1 knockdown represses neuroinflammation and neuronal death in traumatic brain injury by inhibiting microRNA-498 expression.
Jin, Yue; Jiang, Lai; Wang, Yifan; Huang, Yingxue; Yu, Wei; Ma, Xueling.
Afiliação
  • Jin Y; Department of Neurology, The Fourth Affiliated Hospital Of Harbin Medical University, Harbin, Heilongjiang, China.
  • Jiang L; Department of Neurology, The Second Affiliated Hospital Of Harbin Medical University, Harbin, Heilongjiang, China.
  • Wang Y; Department of Neurology, The Fourth Affiliated Hospital Of Harbin Medical University, Harbin, Heilongjiang, China.
  • Huang Y; Department of Neurology, The Fourth Affiliated Hospital Of Harbin Medical University, Harbin, Heilongjiang, China.
  • Yu W; Department of Neurology, The Fourth Affiliated Hospital Of Harbin Medical University, Harbin, Heilongjiang, China.
  • Ma X; Department of Neurology, The Fourth Affiliated Hospital Of Harbin Medical University, Harbin, Heilongjiang, China.
Brain Inj ; 37(7): 611-620, 2023 06 07.
Article em En | MEDLINE | ID: mdl-36951415
OBJECTIVE: Traumatic brain injury (TBI) can result in motor and cognitive dysfunction and is a possible risk factor for the subsequent development of dementia. However, the pathogenesis of TBI remains largely unclear. This study investigated the roles of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in inflammation and neuronal apoptosis following TBI. METHODS: The lncRNA expression profiles in the cerebral cortices of TBI model mice and sham-operated mice were analyzed using microarray. We focused on an upregulated lncRNA, PRR34-AS1, because of its known modulatory role in apoptosis and inflammation. RESULTS: Our findings indicated that the knockdown of PRR34-AS1 inhibited inflammation and neuronal apoptosis and improved long-term neurological function. Using an in vitro, cell-based model of etoposide-induced primary cortical neuronal injury, we demonstrated that PRR34-AS1 levels were higher in injured model cells than in untreated control cells. Silencing of PRR34-AS1 suppressed etoposide-induced apoptosis and the production of inflammatory mediators in primary cortical neurons. PRR34-AS1 directly targets microRNA-498 (miR-498) in primary cortical neurons. Importantly, the inhibition of miR-498 expression counteracted the effects of PRR34-AS1 silencing on neuronal apoptosis and inflammation. CONCLUSIONS: These findings indicate that PRR34-AS1 may be a useful therapeutic target for TBI.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: MicroRNAs / RNA Longo não Codificante / Lesões Encefálicas Traumáticas Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: MicroRNAs / RNA Longo não Codificante / Lesões Encefálicas Traumáticas Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Ano de publicação: 2023 Tipo de documento: Article