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miR-33-5p 对小胶质细胞 M1/M2 极化的保护作用及其机制。

Protective effect of miR-33-5p on the M1/M2 polarization of microglia and the underlying mechanism.

机构信息

Department of Rehabilitation Medicine, Shanghai General Hospital, Shanghai Jiaotong University, Shanghai, China.

Department of Rehabilitation, School of International Medical Technology, Shanghai Sanda University, Shanghai, Pudong, China.

出版信息

Bioengineered. 2022 Apr;13(4):10774-10785. doi: 10.1080/21655979.2022.2061285.

Abstract

This study was aimed to investigate the influence of miR-33-5p on the M1/M2 polarization of microglia and the underlying mechanism. Transcriptome sequencing was performed using microglia from miR-33-5p mimic and control groups. In total, 507 differentially expressed genes, including 314 upregulated genes and 193 downregulated genes, were identified. The subnetwork of module A, which was extracted from the protein-protein interaction networks, mainly contained the downregulated genes. ,and , the members of module-A networks with the highest degrees, possess the potential of being biomarkers of ischemic stroke due to their function in the cell cycle. NFY, a transcription factor, was predicted to have the regulatory relation with nine downregulated genes. Overall, our findings will provide a valuable foundation for genetic mechanisms and treatment studies of ischemic stroke.

摘要

本研究旨在探讨 miR-33-5p 对小胶质细胞 M1/M2 极化的影响及其潜在机制。采用 miR-33-5p 模拟物和对照组的小胶质细胞进行转录组测序。共鉴定出 507 个差异表达基因,其中 314 个上调基因和 193 个下调基因。从蛋白质-蛋白质相互作用网络中提取的模块 A 的子网络主要包含下调基因。模块 A 网络中具有最高度数的、和 ,由于它们在细胞周期中的功能,有可能成为缺血性中风的生物标志物。转录因子 NFY 被预测与 9 个下调基因具有调控关系。总的来说,我们的研究结果将为缺血性中风的遗传机制和治疗研究提供有价值的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/9208509/ff74c0995cf0/KBIE_A_2061285_UF0001_OC.jpg

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