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Molecular mechanism of gonadotropin and prolactin release from pituitary cells

Molecular mechanism of gonadotropin and prolactin release from pituitary cells
垂体细胞释放促性腺激素和催乳素的分子机制
批准号:
60480367
负责人:
AONO Toshihiro
金额:
$2.43万
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (B)
财政年份:
1985
资助国家:
日本
项目状态:
已结题
起止时间:
1985 至 1987

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中文摘要
翻译
促黄体生成素由垂体前叶分泌,催乳素由促性腺激素释放激素分泌。溴隐亭是一种多巴胺激动剂,对治疗催乳素瘤很有用。这种药物不仅能抑制催乳素的释放,还能缩小肿瘤大小。本研究旨在阐明催乳素和黄体生成素分泌的受体后机制,以及多巴胺抑制催乳素释放的分子机制。(方法)以大鼠垂体前叶细胞和HG_3细胞为实验对象。结果(1)毛霉毒素可诱导细胞内钙离子内流并释放催乳素,(2)TRH可促进磷脂酰肌醇代谢中的~(32)>P参入。(3)磷脂酶C被钙激活,将磷脂酰肌醇分解成二酰甘油和接种素三磷酸,诱导催乳素释放。(4)PMA可激活垂体细胞中的蛋白激酶C。PMA刺激黄体生成素和催乳素的分泌。TRH诱导GH_3细胞中催乳素激酶C易位。(5)TRH可促进与~3H-花生四烯酸孵育的垂体细胞磷脂释放花生四烯酸。(6)垂体腺细胞与花生四烯酸孵育后释放催乳素和黄体生成素。(7)尽管5-脂氧合酶产物5-HETE和白三烯可诱导催乳素和黄体生成素的分泌,但环氧合酶产物对催乳素的释放无影响。(8)多巴胺抑制PMA、花生四烯酸、磷脂酶C、乳毒素和5-HETE刺激的催乳素的释放。在无多巴胺受体的GH_3细胞中,多巴胺不能抑制TRH诱导的催乳素释放。(结论)TRH和LHRH分别通过二酰甘油、蛋白激酶和钙、花生四烯酸系统刺激催乳素和黄体生成素。多巴胺会抑制所有这些信号。
英文摘要
LH-RH induces LH from anterior pituitary gland and prolactin is secreted by TRH. Bromocriptine, a dopamine agonist, is useful for the treatment of prolactinoma. This drug not only suppresses prolactin release but also reduces tumor size. The purpose of this research is to clarify the postreceptor mechanism in prolactin and LH secretion, and molecular mechanism of inhibition of prolactin release by dopamine. (METHODS) Rat anterior pituitary cells and HG_3 cell line were used for the experiment. (RESULTS) (1) Maitotoxin induced Ca^<2+> influx into the cells and prolactin release.(2) TRH stimulated-^<32>P incorporation in phosphatidyl inositol turnover. (3)Phospholipase C, Activated by calcium, dissolved phosphatidyl inositol into diacylglycerol and inocitol triphosphate, and induced prolactin release. (4) Protein kinase C in pituitary cells was activated PMA. PMA stimulated LH and prolactin secretion. TRH induced the translocation of prolactin kinase C In GH_3 cells. (5) TRH stimulated arachidonate release from the phospholipids of pituitary cells preincubated with ^3H-arachidonate. (6) Prolactin and LH was released when pituitary cells was incubated with arachidonate. (7) Products of cyclooxygenase has no effects on prolactin release, although 5-HETE and leukotriene, 5-lipoxygenase products, induced prolactin and LH secretion.(8) Dopamine inhibited prolactin release stimulated by PMA, arachidonate, phospholipase C, maitotoxin and 5-HETE. TRH- induced prolactin release was not inhibited by dopamine in GH_3 cells which has no dopamine receptor. (CONCLUSION) TRH and LH-RH stimulated prolactin and LH respectively though diacylglycerol, protein kinase and calcium, arachidonate system. Dopamine inhibit every these signals.
期刊论文(66)
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会议论文
小泉清, 青野敏博, 谷澤修, 伊藤芳晴, 森脇要, 森浩志, 松本圭史: 日本内分泌学会雑誌. 62. 338 (1986)
Kiyoshi Koizumi、Toshihiro Aono、Osamu Tanizawa、Yoshiharu Ito、Kaname Moriwaki、Hiroshi Mori、Keishi Matsumoto:日本内分泌学会杂志 62. 338 (1986)。
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池上博雅, 青野敏博, 小泉清, 大塚志郎, 吉本泰弘, 福井英人, 三宅侃, 谷澤治: 日本産科婦人科学会雑誌. 38. 316 (1986)
Hiromasa Ikegami、Toshihiro Aono、Kiyoshi Koizumi、Shiro Otsuka、Yasuhiro Yoshimoto、Hideto Fukui、Kan Miyake、Osamu Tanizawa:日本妇产科学会杂志 38. 316 (1986)。
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林田美知子, 小泉清, 小池浩司, 池上博雅, 福井英人, 青野敏博, 谷澤修: 日本内分泌学会雑誌. 62. 334 (1986)
Michiko Hayashida、Kiyoshi Koizumi、Koji Koike、Hiromasa Ikegami、Hideto Fukui、Toshihiro Aono、Osamu Tanizawa:日本内分泌学会杂志 62. 334 (1986)。
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