衰老
细胞周期
瘢痕疙瘩
细胞生长
成纤维细胞
细胞
细胞周期检查点
分子生物学
癌症研究
生物
免疫印迹
细胞生物学
化学
细胞培养
病理
医学
基因
遗传学
作者
Jiang Ji,Ye Tian,Yaqun Zhu,Liyuan Zhang,Shengjun Ji,Jian Huan,Xiaozhong Zhou,Jian‐ping Cao
标识
DOI:10.1111/1346-8138.12702
摘要
Abstract Keloids are one of the common refractory conditions in dermatology and aesthetic plastic surgery. The most effective treatment is superficial radiotherapy followed by surgical removal. The rate of recurrence is strongly associated with the total dose of ionizing irradiation, and the underlying mechanism remains unclear. In this study, we used primary keloid fibroblasts ( KF b) isolated from patient samples to investigate the effects of X ‐ray radiation on cell proliferation, cell toxicity and cell cycle, as detected by CCK ‐8 assay kit and flow cytometer. In addition, we examined senescence‐associated β‐galactosidase activity and the associated gene expression using real‐time polymerase chain reaction and western blot in KF b exposed to X ‐ray radiation. X ‐ray radiation inhibited cell proliferation and induced cell senescence in KF b in a dose‐dependent manner. Inhibition of cell proliferation and induction of cellular senescence were mediated by interruption of the cell cycle with an extended G0/G1 phase. Furthermore, the expressions of senescence‐associated genes p21, p16 and p27 were upregulated both at mRNA and protein levels in KF b exposed to X ‐ray radiation. Taken together, our data indicate that X ‐ray radiation may prevent the recurrence of keloids by controlling fibroblast proliferation, arresting the cell cycle and inducing premature cellular senescence.
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