Tissue kallikrein in rat brain and pituitary: regional distribution and estrogen induction in the anterior pituitary.
Tissue kallikrein in rat brain and pituitary: regional distribution and estrogen induction in the anterior pituitary.
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DOI：
10.1210/endo-120-2-475
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发表时间：
1987-02
期刊：
影响因子：
4.8
通讯作者：
J. Chao;L. Chao;C. Swain;J. Tsai;H. Margolius
中科院分区：
文献类型：
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作者：
J. Chao;L. Chao;C. Swain;J. Tsai;H. Margolius
我们已经检测了组织钾化抑制因子和钾化抑制因子mRNA在不同的脑区域与钾化抑制因子直接RIA和核酸杂交使用钾化抑制因子cDNA探针。在直接RIA中，在垂体和松果体、下丘脑、大脑皮层、小脑和脑干中发现大鼠尿钾肽样活性。垂体和松果体钾激肽浓度显著高于其他区域。组织激肽肽浓度仅在垂体中存在显著性差异，雌性大鼠腺体的激肽肽浓度比雄性大鼠高4倍。在脑垂体的所有区域都检测到Kallikrein mrna，女性脑垂体的Kallikrein mrna约为男性脑垂体的4倍。Northern blot分析显示垂体激肽激酶mRNA的性别二态性，其大小与颌下腺和肾脏mRNA相似。在阉割的雄性大鼠中，全垂体激肽素含量降低到对照组的50%，睾酮替代组增加1.7倍，雌二醇17组增加18倍。T4和皮质醇均不影响去势雄性大鼠垂体全钾化肽水平，但睾酮使正常雌性大鼠垂体钾化肽水平降低35%。当分别检查垂体前叶或神经中间体叶提取物时，雌性大鼠的免疫反应性钾化肽分别比雄性大鼠的高10.2倍和1.3倍。苯甲酸雌二醇（30微克/千克）分别使雄性和雌性垂体前叶的钾化肽水平增加90倍和22倍，而雄性和雌性神经中间叶的钾化肽水平仅增加40-50%。dot blot结果显示，17 β -雌二醇可使去势雄性大鼠全垂体中钾化激酶mRNA水平升高5倍。细胞质斑点杂交分析显示，苯甲酸雌二醇使去卵巢大鼠垂体前叶钾化肽mRNA水平升高54倍。数据显示，与尿钾激肽难以区分的组织钾激肽广泛分布于脑和垂体，酶和mRNA的水平在某些中心部位具有可比性。垂体前叶和神经中间叶的钾化肽水平受雌激素的差异调节。
We have detected tissue kallikrein and kallikrein mRNA in various brain regions with a kallikrein direct RIA and with nucleic acid hybridization using a kallikrein cDNA probe. In the direct RIA, rat urinary kallikrein-like activity was found in the pituitary and pineal glands, hypothalamus, cerebral cortex, cerebellum, and brain stem. Pituitary and pineal gland kallikrein concentrations were significantly higher than those in other regions. Only in pituitary was there a significant difference in tissue kallikrein concentration according to sex, with glands from female rats showing levels 4-fold higher than those from male rats. Kallikrein mRNAs were detected in all of the regions and were about 4-fold higher in female than in male pituitary gland. Northern blot analyses show sex dimorphism of pituitary kallikrein mRNA, similar in size to submandibular gland and kidney mRNA. In castrated male rats, whole pituitary kallikrein content was reduced to 50% of the control value and increased 1.7-fold with testosterone replacement and 18-fold with 17 beta-estradiol treatment. Neither T4 nor cortisol affected whole pituitary kallikrein levels in the castrated male rat, but testosterone decreased pituitary kallikrein in normal female rats by 35%. When anterior pituitary or neurointermediate lobe extracts were separately examined, immunoreactive kallikrein was 10.2- and 1.3-fold higher respectively, in female than in male rat lobes. Estradiol benzoate (30 micrograms/kg) administration increased kallikrein levels 90- and 22-fold, respectively, in the anterior pituitary of gonadectomized male and female rats, while it increased by only 40-50% kallikrein levels in the male and female neurointermediate lobe. In dot blot analysis, kallikrein mRNA levels were increased 5-fold by 17 beta-estradiol in the whole pituitary of castrated male rats. In the cytoplasmic dot hybridization analysis, estradiol benzoate treatment increased kallikrein mRNA levels 54-fold in the anterior pituitary of ovariectomized rats. The data show that a tissue kallikrein indistinguishable thus far from a urinary kallikrein is widely distributed in brain and pituitary and that levels of enzyme and mRNA are comparable in certain central sites. Kallikrein levels in the anterior and neurointermediate pituitaries are differentially regulated by estrogen.