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首页> 美国卫生研究院文献>Biochemical Journal >Urokinase- and tissue-type plasminogen activators are suppressed by cortisol in the involuting prostate of castrated rats.
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Urokinase- and tissue-type plasminogen activators are suppressed by cortisol in the involuting prostate of castrated rats.

机译：皮质醇在去势大鼠的渐缩前列腺中抑制了尿激酶和组织型纤溶酶原激活物。

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The effects of cortisol on the inhibition of cell-death processes and suppression of plasminogen-activator (PA) activity during involution of the rat ventral prostate gland were investigated to determine the principal type of PA activated by castration and inhibited by this hormone and whether the mechanism responsible for decreased PA activity involved reductions in enzyme synthesis or increased activity of a PA inhibitor. By using the technique of fibrin-agarose zymography, three bands of PA activity were detected at 4 and 7 days after castration: a major band with a molecular mass of approx. 30 kDa and two minor bands of 48 kDa and 64 kDa. Both the 30 kDa and 48 kDa activities were inhibited with anti-[urokinase-type PA (u-PA)] IgG. The 64 kDa activity was inhibited by anti-[tissue-type PA (t-PA)] IgG. In addition to retarding prostatic involution, daily administration of cortisol to the castrated animals suppressed all three bands of PA activity. A comparison of the pattern of total PA activity and of e.l.i.s.a. estimates of u-PA concentration during the castration-induced rise and after cortisol inhibition indicated a near perfect correlation between the two parameters. Northern-blot analysis using prostatic polyadenylated RNA revealed that the level of u-PA mRNA was highest at 4 and 7 days after castration and that cortisol treatment repressed u-PA mRNA to a level similar to that in non-castrated controls. Neither Northern hybridizations nor reverse zymography detected RNA transcripts or activity corresponding to the PA inhibitor PAI-1 in any of the prostate samples. Western-blot analysis revealed that, although the amount of arginine esterase A, another prostatic proteinase, also increased after castration, the rise in concentration of this protein was not blocked by glucocorticoid administration. Together our findings indicate the following: (1) the predominant form of PA activity induced in the prostate after castration and inhibited by cortisol is a 30 kDa form of u-PA. Although less prominent, t-PA and a 48 kDa form of u-PA follow a similar pattern of induction and inhibition; (2) changes in u-PA activity in response to castration and cortisol treatment are due to alterations in the level of u-PA mRNA and protein rather than in the activity of PAI-1; (3) not all castration-induced proteinases in the prostate are inhibited by cortisol.
机译：研究了皮质醇对大鼠腹侧前列腺退化过程中抑制细胞死亡过程和抑制纤溶酶原激活物（PA）活性的影响，以确定去势激活并被这种激素抑制的PA的主要类型以及是否导致PA活性降低的机理涉及酶合成的减少或PA抑制剂活性的增加。通过使用纤维蛋白琼脂糖酶谱技术，在去势后第4天和第7天检测到3条PA活性带：一条主要条带，分子量约为10。 30 kDa和两个48 kDa和64 kDa的小带。抗[尿激酶型PA（u-PA）] IgG抑制了30 kDa和48 kDa的活性。抗[组织型PA（t-PA）] IgG抑制了64 kDa的活性。除了延缓前列腺退化外，每天向rated割的动物服用皮质醇可抑制PA活动的所有三个谱带。总PA活性和e.l.i.s.a.的模式比较在去势诱发的上升过程中以及皮质醇抑制后，u-PA浓度的估算值表明这两个参数之间具有近乎完美的相关性。使用前列腺多腺苷酸化RNA的Northern印迹分析显示，去势后第4天和第7天，u-PA mRNA的水平最高，而皮质醇治疗将u-PA mRNA的水平抑制到与未-割对照相似的水平。在任何前列腺样品中，Northern杂交和反向酶谱均未检测到与PA抑制剂PAI-1相对应的RNA转录本或活性。 Western印迹分析显示，尽管去势后精氨酸酯酶A（另一种前列腺蛋白酶）的量也增加了，但糖皮质激素的给药并未阻止该蛋白浓度的升高。我们的研究结果共同表明以下几点：（1）去势后在前列腺中诱导并被皮质醇抑制的PA活性的主要形式是30 kDa的u-PA形式。尽管不那么突出，但t-PA和48 kDa形式的u-PA遵循相似的诱导和抑制模式。 （2）去势和皮质醇治疗引起的u-PA活性变化是由于u-PA mRNA和蛋白水平的改变而不是PAI-1活性的改变； （3）并非所有去势诱导的前列腺蛋白酶都被皮质醇抑制。

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