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河北医学  2024, Vol. 30 Issue (6): 886-892    DOI: 10.3969/j.issn.1006-6233.2024.06.02
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Ang-Ⅱ介导的铁死亡参与房颤触发及心衰进展的机制研究
王欣婷, 徐萌萌, 孔雪, 冯洪亮, 杨建
山东省济宁市第三人民医院/济宁市兖州区人民医院心血管内科, 山东 济宁 272000
Mechanism Study on Ang -Ⅱ Mediated Ferroptosis in Triggering Atrial Fibrillation and Progression of Heart Failure
WANG Xinting, XU Mengmeng, KONG Xue, et al
Jining Third People's Hospital / Jining Yanzhou District People's Hospital, Shandong Jining 272000, China
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摘要 目的: 探讨赖氨酸脱甲基酶5B(KDM5B)/增强激活转录因子3(ATF3)信号通路在血管紧张素Ⅱ(Ang-Ⅱ)诱导心脏肥大中的作用。方法: 将小鼠心肌细胞HL-1分为以下处理组:对照组、Ang-Ⅱ组、Ang-Ⅱ+Lv-NC组、Ang-Ⅱ+Lv-KDM5B组和Ang-Ⅱ+Lv-KDM5B KD组。通过蛋白质印迹分析各组细胞中KDM5B、ATF3蛋白表达。通过荧光染色检测细胞内α-肌动蛋白(α-SMA)、Fe2+和活性氧(ROS)水平。结果: 与Ang-Ⅱ+Lv-NC组相比,Ang-Ⅱ+Lv-KDM5B组中HL-1细胞中KDM5B蛋白表达显著增加(P<0.05),和ATF3蛋白表达显著降低(P<0.05),而Ang-Ⅱ+Lv-KDM5B KD组中HL-1细胞中KDM5B蛋白表达显著降低(P<0.05),和ATF3蛋白表达显著增加(P<0.05)。与对照组相比,Ang-Ⅱ组和Ang-Ⅱ+Lv-NC组相对细胞大小、细胞内相对Fe2+荧光强度、相对ROS荧光强度显著增加(P<0.05),和相对细胞活力显著降低(P<0.05)。与Ang-Ⅱ+Lv-NC组相比,Ang-Ⅱ+Lv-KDM5B组相对细胞大小、细胞内相对Fe2+荧光强度、相对ROS荧光强度显著增加(P<0.05),和Ang-Ⅱ+Lv-KDM5B KD组相对细胞大小、细胞内相对Fe2+荧光强度、相对ROS荧光强度显著降低(P<0.05)。结论: KDM5B/ATF3驱动Ang-Ⅱ诱导的心肌肥大的进展,并促进对肥大性应激反应相关的铁死亡。
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关键词 赖氨酸脱甲基酶5B增强激活转录因子3血管紧张素Ⅱ    
AbstractObjective: To investigate the role of lysine demethylase 5B(KDM5B)/ enhanced activated transcription factor 3(ATF3) signaling pathway in angiotensin Ⅱ (Ang-Ⅱ)-induced cardiac hypertrophy.Methods: Mouse cardiomyocytes HL-1 were divided into the following treatment groups: control group, Ang-Ⅱ group, Ang-Ⅱ+Lv-NC group, Ang-Ⅱ+Lv-KDM5B group and Ang-Ⅱ+LV-KDM5KD group. The expression of KDM5B and ATF3 protein in cells of each group was analyzed by protein blot. The intracellular levels of α -actin (α-SMA), Fe2+ and reactive oxygen species (ROS) were detected by fluorescence staining. Results: Compared with Ang-Ⅱ+Lv-NC group, the expression of KDM5B protein in HL-1 cells in Ang-Ⅱ+Lv-KDM5B group increased significantly (P<0.05), and the expression of ATF3 protein decreased significantly (P<0.05), while the expression of KDM5B protein in HL-1 cells in Ang-Ⅱ+Lv-KDM5B KD group decreased significantly (P<0.05). Compared with the control group, the relative cell size, intracellular relative Fe2+ fluorescence intensity and relative ROS fluorescence intensity in Ang-Ⅱ group and Ang-Ⅱ+Lv-NC group increased significantly (P<0.05), and the relative cell viability decreased significantly (P<0.05). Compared with Ang-Ⅱ+Lv-NC group, the relative cell size, intracellular relative Fe2+ fluorescence intensity and relative ROS fluorescence intensity in Ang-Ⅱ+Lv-KDM5B group increased significantly (P<0.05), while the relative cell size, intracellular relative Fe2+ fluorescence intensity and relative ROS fluorescence intensity in Ang-Ⅱ+Lv-KDM5B KD group decreased significantly (P<0.05).Conclusion: KDM5B/ATF3 drives the progress of Ang-Ⅱ-induced myocardial hypertrophy and promotes ferroptosis related to hypertrophic stress response.
Key wordsLysine-specific demethylase 5B    Activating transcription factor 3    Angiotensin Ⅱ
    
基金资助:山东省医药卫生科技项目,(编号:20230301072Q)
通讯作者: 杨建   
引用本文:   
王欣婷, 徐萌萌, 孔雪, 冯洪亮, 杨建. Ang-Ⅱ介导的铁死亡参与房颤触发及心衰进展的机制研究[J]. 河北医学, 2024, 30(6): 886-892.
WANG Xinting, XU Mengmeng, KONG Xue, et al. Mechanism Study on Ang -Ⅱ Mediated Ferroptosis in Triggering Atrial Fibrillation and Progression of Heart Failure. HeBei Med, 2024, 30(6): 886-892.
链接本文:  
http://www.hbyxzzs.cn/CN/10.3969/j.issn.1006-6233.2024.06.02     或     http://www.hbyxzzs.cn/CN/Y2024/V30/I6/886
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