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microRNA-196a attenuates ischemic brain injury in rats by directly targeting high mobility group A1

Dysfunction of the microRNA (miR) network has been indicated as a major regulator in neurological diseases. However, there is limited understanding regarding the functional significance of miRs in ischemic brain injury. In the present study, miR-196a expression was significantly increased in rat bra...

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Detalles Bibliográficos
Autores principales: Hu, Junan, Shen, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6364231/
https://www.ncbi.nlm.nih.gov/pubmed/30783424
http://dx.doi.org/10.3892/etm.2019.7152
Descripción
Sumario:Dysfunction of the microRNA (miR) network has been indicated as a major regulator in neurological diseases. However, there is limited understanding regarding the functional significance of miRs in ischemic brain injury. In the present study, miR-196a expression was significantly increased in rat brains and neurons following transient middle cerebral artery occlusion (MCAO) or oxygen-glucose deprivation, respectively. In addition, repression of miR-196a significantly decreased neuron cell apoptosis and the infarct size in rats subjected to MCAO (P<0.05). Furthermore, miR-196a was indicated to directly target and inhibit high mobility group A1 expression, which indicated a potential role for miR-196a in ischemic brain injury. These findings suggested that miR-196a may be involved in regulating neuronal cell death, thus offering a novel target for the development of therapeutic agents against ischemic brain injury.