刘苏慧, 洪嘉颖, 梁文熙, 农骐郢, 黄永顺. 铅诱导小鼠主动脉内皮细胞向间充质细胞转化[J]. 职业卫生与应急救援, 2025, 43(2): 246-251. DOI: 10.16369/j.oher.issn.1007-1326.2025.240619
引用本文: 刘苏慧, 洪嘉颖, 梁文熙, 农骐郢, 黄永顺. 铅诱导小鼠主动脉内皮细胞向间充质细胞转化[J]. 职业卫生与应急救援, 2025, 43(2): 246-251. DOI: 10.16369/j.oher.issn.1007-1326.2025.240619
LIU Suhui, HONG Jiaying, LIANG Wenxi, NONG Qiying, HUANG Yongshun. Lead-induced transformation of mouse aortic endothelial cells into mesenchymal cells[J]. Occupational Health and Emergency Rescue, 2025, 43(2): 246-251. DOI: 10.16369/j.oher.issn.1007-1326.2025.240619
Citation: LIU Suhui, HONG Jiaying, LIANG Wenxi, NONG Qiying, HUANG Yongshun. Lead-induced transformation of mouse aortic endothelial cells into mesenchymal cells[J]. Occupational Health and Emergency Rescue, 2025, 43(2): 246-251. DOI: 10.16369/j.oher.issn.1007-1326.2025.240619

铅诱导小鼠主动脉内皮细胞向间充质细胞转化

Lead-induced transformation of mouse aortic endothelial cells into mesenchymal cells

  • 摘要:
    目的 探讨铅对小鼠主动脉内皮细胞的活力、形态、功能的影响以及是否诱导细胞发生内皮间充质转化(EndMT)。
    方法 选择小鼠主动脉内皮细胞(MAEC)进行体外培养,实验设对照组和铅暴露组。铅暴露组加入等体积不同浓度的乙酸铅Pb(Ac)2溶液,使终浓度为0~160 μmol/L,置于细胞培养箱内培养24、48 h后,噻唑蓝(MTT)法检测细胞活力,倒置显微镜观察细胞排列及形态,硝酸还原酶法检测细胞培养上清一氧化氮(NO)浓度,免疫印迹法(Western blot)测定细胞中EndMT相关蛋白表达情况包括内皮细胞标志物血小板内皮细胞黏附分子1(CD31)和血管内皮钙黏蛋白(VE-cadherin)以及间质细胞标志物波形蛋白(vimentin)、神经钙黏蛋白(N-cadherin)和α-平滑肌肌动蛋白(α-SMA),实时荧光定量PCR(RT-qPCR)检测细胞中EndMT相关mRNA表达情况。
    结果 与对照组相比,铅暴露组细胞活力明显降低(均P < 0.05),细胞培养上清液中NO浓度上升(P < 0.05)。显微镜下观察,铅暴露组细胞整体排列紊乱,形态由卵圆形向梭形和不规则形转变、“老化”明显。Western blot和RT-qPCR结果均显示,铅暴露组内皮细胞标志物CD31、VE-cadherin的表达水平与对照组相比降低(均P < 0.05),而间充质细胞标志物α-SMA、N-cadherin、vimentin的表达水平与对照组相比升高(均P < 0.05)。
    结论 铅能降低小鼠主动脉内皮细胞活力并改变细胞形态,能诱导内皮细胞向间充质细胞转化。

     

    Abstract:
    Objective To investigate the effects of lead on the viability, morphology, and function of mouse aortic endothelial cells, as well as whether it induces endothelial-mesenchymal transition (EndMT).
    Methods Mouse aortic endothelial cells (MAEC) were cultured in vitro and divided into a control group and a lead exposure group. The lead exposure group was treated with lead acetate Pb (Ac)2 solutions at varying concentrations, with final concentrations of 0 to 160 μmol/L. The cells were incubated for 24 or 48 hours in a cell culture incubator. Cell viability was assessed using the MTT assay, while an inverted microscope was used to observe cell arrangement and morphology. The concentration of nitric oxide (NO) in the cell culture supernatant was determined using the nitrate reductase method. Western blot analysis was conducted to measure the expression of EndMT-related proteins, including endothelial markers platelet endothelial cell adhesion molecule-1(CD31) and vascular endothelial cadherin (VE-cadherin) and mesenchymal markers vimentin, neural cadherin (N-cadherin), and alpha-smooth muscle actin (α-SMA). Furthermore, real-time quantitative PCR (RT-qPCR) was employed to assess the expression of EndMT-related mRNA.
    Results Compared with the control group, the lead exposure group showed significantly reduced cell viability (all P < 0.05) and an increased concentration of NO in the culture supernatant (all P < 0.05). Under the inverted microscope, disordered cell arrangement, morphological changes from oval to spindle-shaped and irregular forms, and apparent "aging" were observed in the MAEC of lead-treated groups. Western blot and RT-qPCR results indicated that the expression levels of endothelial markers (CD31 and VE-cadherin) were significantly decreased(all P < 0.05), while those of mesenchymal markers (α-SMA, N-cadherin, and vimentin) were significantly increased(all P < 0.05) in the lead exposure group compared with the control group.
    Conclusions Lead could reduce the viability of mouse aortic endothelial cells, alter their morphology, and induce their transformation from endothelial to mesenchymal cells.

     

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