The role of growth factors in the suppression of active cell death in the prostate: an hypothesis.

The role of growth factors in the suppression of active cell death in the prostate: an hypothesis.
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生长因子在抑制前列腺主动细胞死亡中的作用:一个假设。

DOI:
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发表时间:
1994
期刊:
Biochemistry and cell biology = Biochimie et biologie cellulaire
影响因子:
--
通讯作者:
M. Tenniswood
M. Tenniswood
中科院分区:
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文献类型:
--
作者:
R. Guenette;M. Tenniswood

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当营养激素5α-二氢睾酮的水平降至抑制细胞凋亡所需的阈值以下时,大鼠的前列腺腹侧就会退化。在诱导前列腺腹侧细胞凋亡的同时,伴随着一些编码蛋白质的mRNAs的稳态水平的增加,这些蛋白质参与了细胞凋亡的后期阶段,从而代表了继发性致死原。这些包括蛋白酶(组织蛋白酶、纤溶酶原激活物和胶原酶)、聚集素、聚(ADP)核糖聚合酶、Tenascin和几个未知基因,以及几个核糖核酸酶和经典的依赖钙、镁(2+)的核酸内切酶。此外,胰岛素样生长因子结合蛋白5(IGFBP-5)被重新诱导。我们认为,IGFBP-5可能通过减弱胰岛素样生长因子信号系统(这是细胞生存所必需的)来触发细胞凋亡过程,因此,IGFBP-5是前列腺中的主要致死物。
Regression of the rat ventral prostate occurs when the level of 5 alpha-dihydrotestosterone, the trophic hormone, drops below the threshold required to suppress apoptosis. The induction of apoptosis in the ventral prostate is accompanied by the increase in the steady-state level of a number of mRNAs coding for proteins that are involved in the latter stages of apoptosis and thus represent secondary thanatogens. These include proteases (cathepsins, plasminogen activators, and collagenase), clusterin, poly(ADP)ribose polymerase, tenascin, and several unidentified genes, as well as several RNases and the classical Ca2+,Mg(2+)-dependent endonuclease. In addition, insulin-like growth-factor-binding protein 5 (IGFBP-5) is induced de novo. We propose that IGFBP-5 may serve to trigger the apoptotic process through the attenuation of the insulin-like growth factor signalling system (which is necessary for cell survival), and as such, represents a primary thanatogen in the prostate.
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