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通过ATG7介导的自能保护人类牙肌纤维细胞免受辐射诱导的亡

Xiumei Zhuang^1,2,3, Xiaoxuan Lin^1,2, Ruogu Xu^1,2

¹Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-Sen University, Guangzhou, China.

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology

|October 25, 2023

概括

纤维化中的抗辐射性涉及肌纤维细胞自活化. 抑制自,特别是ATG7,通过Akt/mTOR途径促进细胞亡,为骨质放射性死提供治疗点.

科学领域:

细胞生物学细胞生物学
在瘤学瘤学.
放射治疗研究放射治疗研究

背景情况:

肌纤维细胞中亡耐药性是辐射诱导的纤维化和大骨核死 (ORNJ) 的关键.
驱动口腔肌纤维细胞中辐射诱导的亡耐药性的分子机制尚不清楚.

研究的目的:

调查自在口腔肌纤维细胞中辐射诱导的亡耐药性中的作用.
探索针对自治疗ORNJ的潜力.

主要方法:

主要培养ORNJ和正常的牙纤维细胞.
在辐射下评估肌纤维细胞标记物 (α-SMA,FAP),细胞活力 (CCK8试验) 和细胞亡 (流细胞计).
对自蛋白 (LC3,ATG7) 和LC3局部化的分析.
对细胞对自抑制剂 (CQ,3-MA) 和ATG7沉默 (siRNA) 的细胞反应的评估.

主要成果:

与正常纤维细胞相比,ORNJ纤维细胞显示α-SMA,FAP,活力增加,辐射后亡降低.
在ORNJ纤维细胞中,辐射上调了LC3-II和ATG7,在CQ治疗时LC3点数增加.
自抑制 (CQ,3-MA) 增强了辐射诱导的亡,并降低了ORNJ纤维细胞的活力.
在被照射的ORNJ纤维细胞中,ATG7沉默降低了LC3-II,增加了亡,并提高了p-AKT/p-mTOR水平.

结论:

人类牙肌纤维细胞通过自细胞激活表现出对辐射诱导的亡的抵抗力.
沉默ATG7抑制了自,促进了亡,并涉及到牙肌纤维细胞中的Akt/mTOR通路.

关键词:

在ATG7中,它是ATG7.灭症 (apoptosis) 是一种死亡的过程.自自是自的过程.辐射辐射辐射的辐射.的肌纤维细胞.

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