Yiming Deng1,2,3, Gaoting Ma1,2,3, Qihao Dong4, Xuan Sun1,2,3, Lian Liu1,2,3, Zhongrong Miao1,2,3, Feng Gao1,2,3. 1. Departments of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, China. 2. China National Clinical Research Center for Neurological Diseases, China. 3. Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China. 4. Central Hospital of Zibo, Department of Neurology, Zibo.
Abstract
AIMS: In previous studies, numerous differential microRNAs (miRNAs) in cerebral ischemic/reperfusion (I/R) injury were identified using the miRNA microarray analysis. However, the relationship between miRNA and cerebral I/R injury remains largely unknown. In this study, we investigated the function and explored the possible mechanism of miR-224-3p in cerebral I/R injury. METHODS: Oxygen glucose deprivation model in N2a cells were used to perform the cerebral I/R injury in vitro. Trypan blue staining, reactive oxygen species (ROS) production, and caspase-3 were measured to evaluate the function of miR-224-3p. RESULTS: Overexpression of miR-224-3p alleviated the apoptosis induced by oxygen glucose deprivation (OGD) and cleaved caspase-3 was significantly reduced. We further provided the possible mechanism that miR-224-3p may protect cells from cerebral I/R injury by targeting FAK family-interacting protein (FIP200). Further rescue experiment proved that overexpression of FIP200 partially blocked the effect of miR-224-3p. CONCLUSIONS: We evaluated the function and mechanism of miR-224-3p in ischemic brain injury. miR-224-3p may serve as a potential target for new therapeutic intervention.
AIMS: In previous studies, numerous differential microRNAs (miRNAs) in cerebral ischemic/reperfusion (I/R) injury were identified using the miRNA microarray analysis. However, the relationship between miRNA and cerebral I/R injury remains largely unknown. In this study, we investigated the function and explored the possible mechanism of miR-224-3p in cerebral I/R injury. METHODS: Oxygen glucose deprivation model in N2a cells were used to perform the cerebral I/R injury in vitro. Trypan blue staining, reactive oxygen species (ROS) production, and caspase-3 were measured to evaluate the function of miR-224-3p. RESULTS: Overexpression of miR-224-3p alleviated the apoptosis induced by oxygen glucose deprivation (OGD) and cleaved caspase-3 was significantly reduced. We further provided the possible mechanism that miR-224-3p may protect cells from cerebral I/R injury by targeting FAK family-interacting protein (FIP200). Further rescue experiment proved that overexpression of FIP200 partially blocked the effect of miR-224-3p. CONCLUSIONS: We evaluated the function and mechanism of miR-224-3p in ischemic brain injury. miR-224-3p may serve as a potential target for new therapeutic intervention.
Authors: Lu Zhang; Cui Jiao; Lingjuan Liu; Aiping Wang; Li Tang; Yi Ren; Peng Huang; Jie Xu; Dingan Mao; Liqun Liu Journal: Front Immunol Date: 2021-06-18 Impact factor: 7.561