miR-34a对高糖状态下小鼠巨噬细胞系RAW264.7极化及炎性因子分泌的影响

doi:10.16352/j.issn.1001-6325.2023.12.1808

基础医学与临床 ›› 2023, Vol. 43 ›› Issue (12): 1808-1813.doi: 10.16352/j.issn.1001-6325.2023.12.1808

miR-34a对高糖状态下小鼠巨噬细胞系RAW264.7极化及炎性因子分泌的影响

张凤云, 赵志浩, 张卓琦^*

徐州医科大学附属医院心内科, 江苏徐州 221000

收稿日期:2022-05-15 修回日期:2022-12-31 出版日期:2023-12-05 发布日期:2023-11-29
通讯作者: ^* zhuoqizhang@sina.com
基金资助:
徐州市推动科技创新项目(KC19062)

Effects of miR-34a on polarization and inflammatory factor content of mouse macrophage cell line RAW264.7 under high glucose conditions

ZHANG Fengyun, ZHAO Zhihao, ZHANG Zhuoqi^*

Department of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221000, China

Received:2022-05-15 Revised:2022-12-31 Online:2023-12-05 Published:2023-11-29
Contact: ^* zhuoqizhang@sina.com

摘要/Abstract

摘要： 目的探讨微小RNA-34a(miR-34a)对高糖条件下小鼠巨噬细胞系极化和炎性因子表达的影响。方法将小鼠巨噬细胞在高糖条件下(25 mmol/L)下培养3至28 d, RT-qPCR检测高糖培养时巨噬细胞中miR-34a表达及M1巨噬细胞标志物(iNOS和MCP-1)和 M2巨噬细胞标志物(Arg-1)的基因表达。转染miR-34a模拟物或抑制剂后,ELISA检测炎性相关因子(IL-6、IL-1β和TNF-α)的分泌。Western blot检测miR-34a靶蛋白1型跨膜糖蛋白Notch1的表达。结果在高糖条件下,巨噬细胞中miR-34a以及M1型巨噬细胞标志物(iNOS和MCP-1)基因表达量逐渐增长。过表达miR-34a后,促炎因子IL-6、IL-1β和TNF-α分泌增加,iNOS和MCP-1 基因表达量也明显增加,而沉默miR-34a的表达后,炎性因子(IL-6、IL-1β和TNF-α)分泌及M1型巨噬细胞标记物(iNOS和MCP-1)的表达量降低(P＜0.05)。沉默Notch1表达后,miR-34a及IL-6、IL-1β和TNF-α分泌及iNOS和MCP-1表达量下降。结论慢性高糖刺激miR-34a表达,后者促进巨噬细胞向M1型极化和促炎因子的分泌。

关键词: miR-34a, 巨噬细胞, 高糖, 极化, 炎性反应

Abstract: Objective To detect the role of miR-34a on macrophage inflammation and polarization under high glucose conditions. Methods Mouse macrophages were collected and cultured during high glucose for 3-28 days. RT-qPCR was used to detect the expression of miR-34a, iNOS, MCP-1 and Arg-1 mRNA. Then miR-34a was over-expressed or silenced, ELISA was used to detect the expression of IL-6, IL-1β,TNF-α and qRT-PCR was used to detect the expression of iNOS and MCP-1 mRNA. Western blot was used to detect the expression of Notch1. Results Expression of miR-34a increased under high glucose conditions in RAW264.7 cells continuously. Over-expression of miR-34a promoted the expression of MCP-1 and iNOS observed by RT-qPCR and increased the expression of IL-6, IL-1β and TNF-α detected by ELISA. Further studies showed that siRNA-Notch1 down-regulated the expression of miR-34a, MCP-1, iNOS, IL-6, IL-1β and TNF-α. Conclusions Chronic high glucose condition stimulates the expression of miR-34a which promotes M1 macrophage polarization and releasing of pro-inflammatory factors.

Key words: miR-34a, macrophage, high glucose, polarization, inflammation

中图分类号:

R587.1

张凤云, 赵志浩, 张卓琦. miR-34a对高糖状态下小鼠巨噬细胞系RAW264.7极化及炎性因子分泌的影响[J]. 基础医学与临床, 2023, 43(12): 1808-1813.

ZHANG Fengyun, ZHAO Zhihao, ZHANG Zhuoqi. Effects of miR-34a on polarization and inflammatory factor content of mouse macrophage cell line RAW264.7 under high glucose conditions[J]. Basic & Clinical Medicine, 2023, 43(12): 1808-1813.

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参考文献 12

[1]	Cho NH, Shaw JE, Karuranga S, et al. IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045[J].Diabetes Res Clin Pract, 2018, 138: 271-281.
[2]	Luc K, Schramm-Luc A, Guzik TJ, et al. Oxidative stress and inflammatory markers in prediabetes and diabetes[J].J Physiol Pharmacol, 2019,70: 10.26402. doi:10.26402/jpp.2019.6.01.
[3]	Hulsmans M, Sam F, Nahrendorf M. Monocyte and macrophage contributions to cardiac remodeling[J].J Mol Cell Cardiol, 2016,93:149-155.
[4]	Zhang B, Yang Y, Yi J, et al. Hyperglycemia modulates M1/M2 macrophage polarization via reactive oxygen species overproduction in ligature-induced periodontitis[J].J Periodontal Res, 2021,56: 991-1005.
[5]	Pan Y, Hui X, Hoo RLC, et al. Adipocyte-secreted exosomal microRNA-34a inhibits M2 macrophage polarization to promote obesity-induced adipose inflammation[J]. J Clin Invest, 2019,129: 834-849.
[6]	Ishibashi Y, Matsui T, Maeda S, et al. Advanced glycation end products evoke endothelial cell damage by stimulating soluble dipeptidyl peptidase-4 production and its interaction with mannose 6-phosphate/insulin-like growth factor Ⅱ receptor [J].Cardiovasc Diabetol,2013,12: 125. doi:10.1186/1475-2840-12-125.
[7]	Wen Y, Gu J, Li SL, et al. Elevated glucose and diabetes promote interleukin-12 cytokine gene expression in mouse macrophages[J]. Endocrinology, 2006,147: 2518-2525.
[8]	Shapouri-Moghaddam A, Mohammadian S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease[J].J Cell Physiol, 2018, 233: 6425-6440.
[9]	Raucci A, Macrì F, Castiglione S, et al. MicroRNA-34a: the bad guy in age-related vascular diseases[J].Cell Mol Life Sci, 2021,78:7355-7378.
[10]	游慧, 康海军, 陈方,等. 高血压视网膜病变患者外周血单个核细胞Notch1水平及其与血管内皮功能的相关性[J]. 基础医学与临床, 2022, 42: 1528-1532.
[11]	Xu J, Chi F, Guo T, et al. NOTCH reprograms mitochondrial metabolism for proinflammatory macrophage activa-tion[J]. J Clin Invest,2015,125:1579-1590.
[12]	Ge Y, Huang M, Ma YF. The effects of microRNA-34a regulating Notch-1/NF-κB signaling pathway on lipopolysaccharide-induced human umbilical vein endothelial cells[J].World J Emerg Med,2017,8: 292-296.

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miR-34a对高糖状态下小鼠巨噬细胞系RAW264.7极化及炎性因子分泌的影响

Effects of miR-34a on polarization and inflammatory factor content of mouse macrophage cell line RAW264.7 under high glucose conditions

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