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首页> 外文期刊>International Journal of Radiation Biology: Covering the Physical, Chemical, Biological, and Medical Effects of Ionizing and Non-ionizing Radiations >Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts
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Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts

机译：辐射诱导的FANCD2原代成纤维细胞中的有丝分裂灾难

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Purpose: As the Fanconi anemia (FA) pathway is required for appropriate cell cycle progression through mitosis and the completion of cell division, the aim of the present study was to determine the destiny of FA cells after irradiation in vitro and to elucidate any difference in radiosensitivity between FA and control cells. Materials and methods: Analyses of phosphorylated histone H2AX (γ-H2AX) foci, micronuclei formation and cell cycle analysis were performed in unirradiated (0 min) and irradiated primary FA fibroblasts and in a control group at different post-irradiation times (30 min, 2 h, 5 h and 24 h). Results: The accumulation of γ-H2AX foci in irradiated FA fibroblasts was observed. At 24 h post-irradiation, 57% of FA cells were γ-H2AX foci-positive, significantly higher than in the control (p < 0.01). The cell cycle analysis has shown the transient G2/M arrest in irradiated FA fibroblasts. The portion of cells in the G2/M phase showed initial increase at 30 min post-irradiation and afterwards decreased over time reaching the pretreatment level 24 h after irradiation. Irradiated FA fibroblasts progressed to abnormal mitosis, as is shown by the production of cells with different nuclear morphologies from binucleated to multinucleated surrounded with micronuclei, and also by a high percentage of foci-positive micronuclei. The majority of radiation-induced micronuclei were γ-H2AX foci-positive, indicating that radiation-induced micronuclei contain fragments of damaged chromosomes. In contrast, in the control group, most of the micronuclei were classified as γ-H2AX foci-negative, which indicates that cells with unrepaired damage were blocked before entering mitosis. Conclusion: The results clearly indicate that mitotic catastrophe might be an important cell-death mechanism involved in the response of FA fibroblasts to ionizing radiation.
机译：目的：由于范科尼贫血（FA）途径是通过有丝分裂和完成细胞分裂而适当的细胞周期进程所必需的，因此本研究的目的是确定体外照射后FA细胞的命运，并阐明在FA和对照细胞之间的放射敏感性。材料和方法：在未辐照（0分钟）和辐照的原代FA成纤维细胞中以及对照组中，在不同的辐照后时间（30分钟， 2小时，5小时和24小时）。结果：观察到辐照的FA成纤维细胞中γ-H2AX病灶的积累。辐照后24 h，57％的FA细胞为γ-H2AX病灶阳性，显着高于对照组（p <0.01）。细胞周期分析表明，经辐照的FA成纤维细胞中G2 / M的瞬时停滞。 G2 / M期的部分细胞在辐照后30分钟显示出最初的增加，随后随着时间的推移而减少，达到辐照后24 h的预处理水平。辐照过的FA成纤维细胞进展为异常有丝分裂，这表现为具有不同核形态（从双核到多核被微核包围）的细胞生成，以及高百分比的病灶阳性微核。辐射诱导的微核大多数为γ-H2AX病灶阳性，表明辐射诱导的微核含有受损染色体的片段。相反，在对照组中，大多数微核被归类为γ-H2AX病灶阴性，这表明损伤未修复的细胞在进入有丝分裂之前被阻断。结论：结果清楚地表明，有丝分裂灾难可能是FA成纤维细胞对电离辐射反应的重要细胞死亡机制。

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