Strain differences and inheritance of angiogenic versus angiostatic activity in oestrogen-induced rat pituitary tumours.
Strain differences and inheritance of angiogenic versus angiostatic activity in oestrogen-induced rat pituitary tumours.
复制标题
雌激素诱导的大鼠垂体肿瘤中血管生成与血管抑制活性的菌株差异和遗传。
DOI：
10.1023/a:1021550211921
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发表时间：
2002
期刊：
影响因子：
9.8
通讯作者：
Wendell,DouglasL
中科院分区：
文献类型：
--
作者：
Pandey,Jyotsna;Cracchiolo,Danny;Hansen,FayM;Wendell,DouglasL
在这项研究中，我们研究了Fischer 344 (F344)（肿瘤易感）和Brown Norway（肿瘤耐药）菌株的F1杂交株（F1）雌激素诱导的大鼠垂体肿瘤血管生成/出血表型的控制。f1在慢性雌激素治疗后形成垂体瘤，但微血管计数（MVC）并不比未治疗时大。换句话说，在雌激素诱导的肿瘤生长过程中，F1MVC与组织生长保持同步。另一方面，F344在大垂体瘤生长过程中，经慢性雌激素治疗后，MVC显著增加（P= 0.002）。f1对照的血管系统表现出介于亲本株之间的特征，而雌激素处理的f1垂体有明显的变化，与血管重构或血管生成活性相称，并伴有退行性变化。此外，雌激素处理的f1不会形成雌激素处理的F344所特有的出血性湖泊。我们得出结论，F1具有50-50的肿瘤易感性和肿瘤抗性等位基因的遗传组成，在缺乏有效的血管生成刺激时显示血管抑制活性的丧失。因此，它无法“切换”到血管生成表型。
In this study we investigated the control of the angiogenic/haemorrhagic phenotype of oestrogen-induced rat pituitary tumours of an F1hybrid (F1) of Fischer 344 (F344) (tumour susceptible) and Brown Norway (tumour resistant) strains. F1forms a pituitary tumour upon chronic oestrogen treatment, but microvessel count (MVC) is no greater than untreated. In other words, F1MVC keeps pace with tissue growth during growth of an oestrogen-induced tumour. On the other hand, F344 showed a significant increase in MVC (P= 0.002) upon chronic oestrogen treatment during growth of a large pituitary tumour. F1control vasculature showed features intermediate between the parent strains, while oestrogen-treated F1pituitary has pronounced changes commensurate with vascular remodelling or angiogenic activity, along with regressive changes. In addition, oestrogen-treated F1does not form the haemorrhagic lakes characteristic of oestrogen-treated F344. We conclude that F1, which has a 50-50 genetic composition of the tumour susceptibility and tumour resistance alleles, shows loss of angiostatic activity in the absence of an effective angiogenic stimulus. As a result it is unable to make the 'switch’ to the angiogenic phenotype.