表达多瘤中T瘤基因的内皮质瘤细胞通过宿主细胞招募诱导血管瘤
R L Williams1, W Risau, H G Zerwes
1European Molecular Biology Laboratory, Heidelberg, Federal Republic of Germany.
Cell
|June 16, 1989
概括
聚瘤中T瘤基因表达性内皮质瘤细胞通过招募宿主内皮细胞迅速诱导血管瘤. 这些瘤在成年小鼠中形成稳定的结构,需要持续存在的内皮质瘤细胞来维持.
科学领域:
- 在瘤学瘤学.
- 血管生物学 血管生物学
- 发育生物学 发展生物学
背景情况:
- 众所周知,表达多瘤中T瘤基因的内皮质瘤细胞可诱导瘤.
- 血管瘤是良性血管瘤,可以发生在各种物种中.
研究的目的:
- 研究内皮质瘤细胞诱导血瘤形成的机制.
- 描述诱导血瘤的细胞组成和行为.
- 确定宿主细胞增殖和辅原体在血瘤发育中的作用.
主要方法:
- 向各种动物模型 (老鼠,老鼠,小,长) 注射表达多瘤中T瘤基因的小鼠内皮瘤细胞.
- 随着时间的推移,监测血瘤的发展,扩张和血管干扰.
- 血管瘤细胞组成的组织学分析,识别内皮细胞起源.
- 在体外评估内皮质瘤细胞分泌的内皮质辅激素和宿主细胞增殖诱导.
主要成果:
- 血瘤在胚胎和新生小鼠中迅速形成,导致血管干扰和死亡.
- 在成年小鼠中,血管瘤在5天内发展成类似良性人体血管瘤的稳定结构.
- 血管瘤内95%以上的内皮细胞来自宿主.
- 没有观察到由内皮质瘤细胞诱导宿主细胞增殖或内皮质辅激素的分泌.
- 持续存在的内皮质瘤细胞是维持血瘤所必需的.
结论:
- 表达多瘤中T瘤基因的内皮质瘤细胞是快速形成血瘤的有力剂.
- 血管瘤诱导是通过招募非增殖宿主内皮细胞发生的,而不是通过刺激宿主细胞增殖.
- 成年小鼠中血管瘤的稳定性表明,瘤细胞与宿主环境之间存在复杂的相互作用.
- 这些发现提供了关于血管瘤的病变发生和潜在的治疗策略的见解.
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