| 伊如罕,陆雪,蔡恬静,等.Caveolin-1在电离辐射诱导血管内皮细胞早衰中的作用研究[J].中华放射医学与防护杂志,2025,45(3):163-169.Yi Ruhan,Lu Xue,Cai Tianjing,et al.Study on the role of Caveolin-1 in ionizing radiation-induced premature senescence of vascular endothelial cells[J].Chin J Radiol Med Prot,2025,45(3):163-169 |
| Caveolin-1在电离辐射诱导血管内皮细胞早衰中的作用研究 |
| Study on the role of Caveolin-1 in ionizing radiation-induced premature senescence of vascular endothelial cells |
| 投稿时间：2024-11-14 |
| DOI：10.3760/cma.j.cn112271-20241114-00439 |
| 中文关键词: 电离辐射 X射线 血管内皮细胞 早衰 Caveolin-1 |
| 英文关键词:Irradiation X-rays Vascular endothelial cells Premature senescence Caveolin-1 |
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| 中文摘要: |
| 目的 探讨Caveolin-1(CAV-1)在电离辐射诱导血管内皮细胞早衰中的作用机制。方法 在人微血管内皮细胞(HMEC-1)中,通过慢病毒转染方法,利用嘌呤霉素筛选构建稳定敲低CAV-1的细胞模型,根据是否感染慢病毒shRNA-CAV-1将细胞分为对照(NC)组和sh-CAV-1组。采用Western blot检测CAV-1蛋白表达水平。0、2、4 Gy X射线照射人微血管内皮细胞后24、48和72 h,利用β-半乳糖苷酶染色试剂盒检测细胞β-半乳糖苷酶染色情况;利用Western blot检测衰老标志蛋白p53蛋白和p21蛋白表达情况;用CCK-8试剂盒检测细胞活力变化;通过血管生成实验检测血管内皮细胞功能。结果 2、4 Gy X射线照射后48 h,CAV-1蛋白表达显著下降(t=3.50、3.89,P< 0.05)。0、2、4 Gy X射线照射后,与NC组相比,sh-CAV-1组 β-半乳糖苷酶染色显著增加(t=12.91、11.54、6.04,P< 0.05);在HMEC-1细胞中敲低CAV-1, 细胞衰老相关蛋白p53表达水平显著下降(t=4.09、3.13、3.43,P< 0.05),p21蛋白表达水平显著增加(t=-3.63、-3.33、-3.06,P< 0.05)。与NC组相比,CAV-1敲低的HMEC-1细胞活力显著下降(t=2.97~25.89,P< 0.05);血管生成能力降低(t=3.39~39.68,P< 0.05)。结论 CAV-1通过正向调控p53,负调控p21参与电离辐射诱导血管内皮细胞早衰发生过程。 |
| 英文摘要: |
| Objective To explore the role of Caveolin-1 (CAV-1) in radiation-induced premature senescence of vascular endothelial cells. Methods A cell model with stable knockdown of CAV-1 was constructed in human microvascular endothelial cells (HMEC-1) by lentiviral transfection using puromycin screening. The cells were divided into NC group and sh-CAV-1 group based on whether they were infected with lentivirus shRNA-CAV-1. The protein expression levels of CAV-1, p53 and p21 were detected by Western blot at 24, 48, and 72 h after 0, 2, and 4 Gy X-ray irradiation. The β-galactosidase staining kit was used to detect β-galactosidase in cells. CCK-8 kit was used to detect cell viability, and vascular endothelial cell function was detected by vascular tube-forming assay. Results CAV-1 protein expression was significantly decreased at 48 h after 2 and 4 Gy X-ray irradiation (t= 3.50, 3.89, P < 0.05), and β-galactosidase in sh-CAV-1 group was significantly increased at 72 h after 0, 2 and 4 Gy X-ray irradiation (t= 12.91, 11.54, 6.04, P< 0.05) compared with the NC group. Knockdown of CAV-1 resulted in the decrease in the expression level of the cellular senescence-associated protein p53 protein (t= 4.09, 3.13, 3.43, P< 0.05), but increase in the expression level of p21 protein (t= -3.63, -3.33, -3.06, P< 0.05). Compared with the NC group, knockdown CAV-1 significantly decreased cell viability (t= 2.97-25.89, P< 0.05) and reduced vessel-forming capacity (t= 3.39-39.68, P< 0.05). Conclusions CAV-1 is involved in the process of radiation-induced premature senescence of vascular endothelial cells through positive regulation of p53 and negative regulation of p21. |
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