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Overexpression of microRNA-381-3p ameliorates hypoxia/ischemia-induced neuronal damage and microglial inflammation via regulating the C-C chemokine receptor type 2 /nuclear transcription factor-kappa B axis.
Che, Yuanmei; He, Jianglong; Li, Xiaopeng; Wu, Daxian; Zhang, Yi; Yuan, Guicai.
Afiliación
  • Che Y; Department of Infection, The First Affiliated Hospital of Nanchang University, Nanchang, China.
  • He J; Department of Infection, The First Affiliated Hospital of Nanchang University, Nanchang, China.
  • Li X; Department of Infection, The First Affiliated Hospital of Nanchang University, Nanchang, China.
  • Wu D; Department of Infection, The First Affiliated Hospital of Nanchang University, Nanchang, China.
  • Zhang Y; Department of Infection, The First Affiliated Hospital of Nanchang University, Nanchang, China.
  • Yuan G; Department of Infection, The Second Affiliated Hospital of Yichun University, Yichun, China.
Bioengineered ; 13(3): 6839-6855, 2022 03.
Article en En | MEDLINE | ID: mdl-35246016
microRNAs, as small endogenous RNAs, influence umpteen sophisticated cellular biological functions regarding neurodegenerative and cerebrovascular diseases. Here, we interrogated miR-381-3p's influence on BV2 activation and neurotoxicity in ischemic and hypoxic environment. Oxygen-glucose deprivation (OGD) was adopted to induce microglial activation and HT-22 neuron damage. Quantitative polymerase chain reaction (qRT-PCR) was taken to check miR-381-3p expression in OGD-elicited BV2 cells and HT-22 neurons. It transpired that miR-381-3p expression was lowered in BV2 cells and HT-22 cells elicited by OGD. miR-381-3p up-regulation remarkably hampered inflammatory mediator expression in BV2 cells induced by OGD and weakened HT22 neuron apoptosis. In vivo, miR-381-3p expression was abated in HI rats' ischemic lesions, and miR-381-3p up-regulation could ameliorate inflammation and neuron apoptosis in their brain. C-C chemokine receptor type 2 (CCR2) was identified as the downstream target of miR-381-3p, and miR-381-3p suppressed the CCR2/NF-κB pathway to mitigate microglial activation and neurotoxicity. Therefore, we believed that miR-381-3p overexpression exerts anti-inflammation and anti-apoptosis in ischemic brain injury by targeting CCR2.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: FN-kappa B / MicroARNs Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Bioengineered Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: FN-kappa B / MicroARNs Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Bioengineered Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos