增加的蛋白质分解活性是表达中T瘤基因的内皮细胞异常形态遗传行为的原因
R Montesano1, M S Pepper, U Möhle-Steinlein
1Department of Morphology, University Medical Center, Geneva, Switzerland.
Cell
|August 10, 1990
概括
多瘤病毒中间T (mT) 瘤基因破坏了血管发育,导致血管瘤. 控制纤维溶解活性是正常血管形成的关键,可以调节血管生成.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 血管生物学 血管生物学
背景情况:
- 多瘤病毒中间T (mT) 瘤基因驱动异常的血管发育,导致内皮瘤 (血管瘤).
- 了解mT诱导的血管形背后的分子机制至关重要.
研究的目的:
- 为了研究表达mt瘤基因的内皮细胞的体外形态遗传特性.
- 阐明蛋白质活性在mT诱导的血管异常中的作用.
主要方法:
- 在纤维素凝中培养表达mT的内皮质瘤 (End) 细胞.
- 通过测量尿素酶类型的塑原激活剂和塑原激活剂抑制剂水平来评估纤维解质活性.
- 用血清蛋白酶抑制剂治疗终端细胞.
主要成果:
- 末端细胞在纤维素凝中形成了类似血管瘤的囊性结构.
- 终端细胞表现出高的纤维解质活性,这是由于尿激酶类型等离子素激活剂的增加和等离子素激活剂抑制剂的减少.
- 血清蛋白酶抑制剂使终端细胞行为正常化,促进了毛细管状管体的形成.
结论:
- 严格控制的蛋白质分解活性对于正常的血管形态发生是必不可少的.
- 生理蛋白酶抑制剂在血管生成中起着关键的调节作用.
- 失调的纤维素分解有助于瘤基因诱导的血管瘤.
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