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].Chinese Journal of Radiological Medicine and Protection,2025,45(3):163-169
Study on the role of Caveolin-1 in ionizing radiation-induced premature senescence of vascular endothelial cells
Received:November 14, 2024  
DOI:10.3760/cma.j.cn112271-20241114-00439
KeyWords:Irradiation  X-rays  Vascular endothelial cells  Premature senescence  Caveolin-1
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Author NameAffiliationE-mail
Yi Ruhan Key Laboratory of Radiological Protection and Nuclear Emergency, China CDC, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, Beijing 100088, China  
Lu Xue Key Laboratory of Radiological Protection and Nuclear Emergency, China CDC, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, Beijing 100088, China  
Cai Tianjing Key Laboratory of Radiological Protection and Nuclear Emergency, China CDC, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, Beijing 100088, China  
Gao Ling Key Laboratory of Radiological Protection and Nuclear Emergency, China CDC, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, Beijing 100088, China gaoling@nirp.chinacdc.cn 
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Abstract::
      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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