Yan Juan,Liu Qingjie,Tian Mei,et al.Premature senescence and the protein expressions of P53 and P16 in HaCaT cells after UVB exposure[J].Chinese Journal of Radiological Medicine and Protection,2020,40(4):284-289
Premature senescence and the protein expressions of P53 and P16 in HaCaT cells after UVB exposure
Received:October 16, 2019  
DOI:10.3760/cma.j.issn.0254-5098.2020.04.007
KeyWords:Ultraviolet B  Premature senescence  Keratinocytes  P53  P16
FundProject:北京市自然科学基金(7162137,7202139)
Author NameAffiliationE-mail
Yan Juan 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  
Liu Qingjie 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  
Tian Mei 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  
Li Shuang 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  
Zhao Hua 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  
Tian Xuelei 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  
Chen Deqing 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 gaolingxinxin@126.com 
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Abstract::
      Objective To explore the effects of ultraviolet B (UVB) on the premature senescence of human immortalized keratinocytes HaCaT cells and the possible underlying molecular mechanism. Methods HaCaT cells were exposed with UVB of different doses (20, 50, 80 and 100 mJ/cm2). At 72 h after exposure, cellular morphology was observed by Giemsa staining, cell proliferation was detected by clone formation assay, and the proportion of premature senescence cells was detected by β-galactosidase staining. The number change of lysosomes was detected by Lyso-Tracker Red fluorescence probe at 24, 48 and 72 h after exposure. Cell migration was measured by scratch test at 24 h and 48 h after exposure. The protein expressions of p53 and p16 related to premature senescence were detected by Western blot assay at 72 h after exposure. Results After UVB exposure, HaCaT cells showed a premature senescence phenotype. At 72 h after exposure, the cell volume increased (F=115.18,P<0.05), the cell proliferation ability decreased (F=410.32, P<0.05), the activity of β-galactosidase increased (F=16.31,P<0.05), and the expressions of P53 and P16 increased. In addition, the number of lysosomes increased at 24, 48, and 72 h after exposure (F=17.65, 38.36, 13.66, P<0.05),and cell migration capacity was inhibited at 24 and 48 h after exposure (F=8.21, 11.48, P<0.05). Conclusions UVB exposure can induce premature senescence of HaCaT cells by increasing the expression of p53 and p16 proteins.
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