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Cell Type-specific Gene Expression Profiling in the Mouse Liver
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描述了肝细胞中老化诱导的功能变化的异质性
Pavitra Kumar1, Mohsin Hassan1, Frank Tacke1
1Department of Hepatology and Gastroenterology, Medizinische Klinik m. S. Hepatologie und Gastroenterologie, Charité, Universitätsmedizin Berlin, Campus Virchow-Klinikum (CVK) and Campus Charité Mitte (CCM), Augustenburger Platz 1, Forum 4, Raum 2.0704a, 13353, Berlin, Germany.
Cellular and molecular life sciences : CMLS
|April 29, 2024
概括
肝细胞中的细胞衰老是压力特异性的,观察到不同的分子模式和生物能变化. doxorubicin 和 cisplatin 是强大的诱导剂,突出显示了肝细胞衰老的异质性.
科学领域:
- 肝病学和细胞生物学
- 疾病的分子和细胞机制.
- 肝脏有机技术 肝脏有机技术
背景情况:
- 肝细胞中的细胞衰老通过细胞循环停止,改变的生物能量和炎症导致肝病.
- 衰老表型是异质的,受到诱导应激因素和细胞类型的影响.
- 了解这些变异对于肝病研究至关重要.
研究的目的:
- 在初级小鼠肝细胞 (PMH) 和肝细胞衍生的肝器官 (HepOrgs) 中特征压力特异性的衰老表型.
- 分析与不同衰老诱导剂相关的分子模式和细胞生物能学.
- 为了比较2D培养中的衰老诱导与3D有机体.
主要方法:
- 原始小鼠肝细胞和肝脏器官被培养并接受各种衰老诱导物 (DNA损伤,氧化应激,端粒抑制等). ) 的情况.
- 使用SA-β-galactosidase活性,免疫光,免疫阻塞,SASP分析和细胞生物能学来评估衰老.
- 具体的诱导剂包括多克索鲁比,西斯普拉丁,埃托波西德,H2O2,乙醇,BIBR-1532,努特林-3a,5-阿扎西提丁,银胺和氧尿素.
主要成果:
- 每个衰老诱导剂都在肝细胞中引起了一组独特的衰老标记物.
- 大多数诱导剂的SA-β-银酸酶活性增加,除了氨酸urea和乙醇.
- CCL2和IL-10一直是上调的SASP因子,而等离子体激活剂抑制剂-1则是下调的.
- 诱导DNA损伤的诱导剂激活了DNA损伤反应;多克索鲁比,西斯普拉丁和银胺显著减少了细胞周期标记物.
- 由DNA损伤引起的衰老将生物能量从糖解转移到氧化酸化.
- 与PMH相比,HepOrgs的SASP基因表达率较高,gH2A.X,p53和p21水平增加.
结论:
- 衰老诱导剂在PMH中激活了不同的标记组合,其中多克索鲁比辛,西斯普拉丁和H2O2具有高度有效性.
- 所有测试的诱导因子都诱导了DNA损伤反应和线粒体功能障碍,独立于MAPK/AKT信号传递.
- 在HepOrgs中诱导衰老反映了PMH,但表现出放大了SASP反应.
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