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

Autor: Che, Yuanmei, He, Jianglong, Li, Xiaopeng, Wu, Daxian, Zhang, Yi, Yuan, Guicai
Rok vydání: 2022
Předmět:
DOI: 10.6084/m9.figshare.19311123.v1
Popis: 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-��B 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
Databáze: OpenAIRE