Cellular mechanisms of estrogen- and dopamine-induced control of glandular kallikrein in the anterior pituitary of the rat.
Cellular mechanisms of estrogen- and dopamine-induced control of glandular kallikrein in the anterior pituitary of the rat.
复制标题
雌激素和多巴胺诱导的大鼠垂体前叶腺激肽释放酶的细胞机制。
DOI：
10.1007/bf00314538
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发表时间：
1993
影响因子：
3.6
通讯作者：
Vio,CP
中科院分区：
文献类型：
--
作者：
Roa,JP;Powers,CA;Silva,R;Vio,CP
腺激肽释放酶（GK，一种胰蛋白酶样丝氨酸蛋白酶）在大鼠垂体催乳素细胞中表现出雌激素诱导作用和多巴胺抑制作用。类固醇诱导可能反映选择性增加特定蛋白质合成的主要作用，或者可能是类固醇诱导的表型转变继发的广泛细胞反应的一部分。本研究采用定量免疫细胞化学方法研究了雌激素和多巴胺能控制泌乳素 GK 的细胞机制。切除卵巢的大鼠的垂体几乎没有表现出 GK 染色。雌二醇治疗 10 天后，垂体质量、泌乳素细胞百分比（表明泌乳素细胞增殖）和 GK 阳性细胞百分比呈剂量依赖性增加。此外，GK 染色强度取决于雌二醇剂量，在 5 μg 至 50 μg/48 小时之间增加 4 倍。在没有雌二醇的情况下，用氟哌啶醇（2.5 mg/kg/24 h）阻断多巴胺受体会在 46% 的泌乳素细胞中引发微弱的 GK 免疫染色，而低剂量而非高剂量的雌二醇会显着增强 GK 染色强度。结果表明，GK 诱导是雌激素的主要作用，而不是继发于表型转变：雌激素诱导的泌乳素增殖增强了诱导作用。多巴胺能系统通过低雌二醇水平强烈抑制 GK 诱导。这种多巴胺能调节可能会将催乳素 GK 的诱导转变为与高雌二醇水平或多巴胺能张力相关的生理事件。
Glandular kallikrein (GK, a trypsin-like serine protease) exhibits estrogen induction and dopamine repression in rat pituitary lactotrophs. Steroid induction may reflect primary actions to increase selectively the synthesis of specific proteins, or may be part of broad cellular responses secondary to steroid-induced phenotype transitions. This study examined the cellular mechanisms underlying estrogen and dopaminergic control of lactotroph GK using a quantified immunocytochemical approach. Pituitaries from ovariectomized rats exhibited little GK staining. Estradiol treatment for 10 days produced dose-dependent increases in pituitary mass, the percentage of lactotrophs (indicating lactotroph proliferation) and the percentage of GK-positive cells. Also, GK staining intensity was dependent upon estradiol dose, increasing 4-fold between 5 μg and 50 μg/48 h. Dopamine receptor blockade with haloperidol (2.5 mg/kg/24 h) elicited weak GK immunostaining in 46% of the lactotrophs in the absence of estradiol, and markedly potentiated GK staining intensity elicited with low but not high doses of estradiol. The results suggest that GK induction is a primary estrogen effect, and is not secondary to a phenotype transition: the induction is enhanced by estrogen-induced lactotroph proliferation. Dopaminergic systems strongly inhibit GK induction by low estradiol levels. This dopaminergic modulation may shift the induction of lactotroph GK to physiological events associated with high estradiol levels or low dopaminergic tone.