Common hormones and mechanisms of luteal regression, ovulation and follicular atresia.
Common hormones and mechanisms of luteal regression, ovulation and follicular atresia.
批准号:
08671909
负责人:
ENDO Toshiaki
金额:
$1.41万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1996
资助国家:
日本
项目状态:
已结题
起止时间:
1996 至 1997
中文摘要
我们研究了黄体退化、排卵和卵泡闭锁的常见激素及其机制。我们之前报道过,在溴隐碱(Brom)治疗后,催乳素(PRL)治疗超排卵大鼠引起结构性黄体溶解,并且这种治疗刺激了累及黄体的基质金属蛋白酶活性并引起细胞凋亡。我们旨在探讨除PRL外的其他激素是否会引起大鼠结构性黄体溶解,并探讨人类黄体退化的机制。我们得到了一些优秀的数据如下。Brom处理后的生长激素处理通过MMP激活和细胞凋亡引起结构性黄体溶解。注射hCG后第5天至第9天使用促性腺激素释放激素激动剂(GnRHa)也引起大鼠结构性黄体溶解。明胶酶谱分析、Northem blot分析显示,GnRHa处理刺激了MMP-2、MT-MMP活性。黄体晚期提取物的MMP-2、MT1-MMP活性明显高于其他期提取物。黄体组织金属蛋白酶抑制剂(TIMP)-1的表达在黄体晚期降低。而TIMP-2的表达在黄体晚期略有升高。可能如先前在其他细胞中报道的那样,在TIMP-2存在的情况下,MT1-MMP激活了前mmp -2。很明显,黄体退化、排卵和卵泡闭锁具有上述相同的机制。
英文摘要
We investigated common hormones and mechanisms of luteal regression, ovulation and follicular atresia. We previously reported that prolactin (PRL) treatment following bromocryptine (Brom) treatment to superovulated rats caused structural luteolysis, and that this treatment stimulated matrix metalloproteinase activity in involuted corpus luteum and caused apoptosis.We designed to investigate whether other hormones except PRL may cause structural luteolysis in rats, and also investigated about mechanisms of luteal regression in human. We got some exellent data as below.Growth hormone treatment following Brom treatment caused structural luteolysis by MMP activation and apoptosis. Gonadotropin releasing hormone agonist (GnRHa) treatment from day 5 through day 9 after hCG injection also caused structural luteolysis in rats. Gelatin zymography, Northem blot analysis revealed that GnRHa treatment stimulated MMP-2, MT-MMP activity.Extracts of human corpus luteum of late luteal phase had much more activities of MMP-2, MT1-MMP than those of other stages. Tissue inhibitor of metalloproteinse (TIMP)-1 expression of corpus luteum decreased at late luteal phase. However, TIMP-2 expression slightly increased at late luteal phase compared with other stages. It is possible that MT1-MMP activates pro-MMP-2 under the existence of TIMP-2 as previously reported in other kinds of cells.It became clear that luteal regression, ovulation and follicular atresia have same kinds of mechanisms as mentioned above.
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Tamotsu Kiya: "Apoptosis and PCNA expression induced by prolactin in structural involution of the rat corpus lutlteum" Journal of Endocrinological Investigation. (in press). (1998)
Tamotsu Kiya:“催乳素在大鼠黄体结构退化中诱导细胞凋亡和 PCNA 表达”内分泌研究杂志。
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Tamotsue Kiya: "Cell cycle-dependent apoptosis in prolactin-induced structural luteolysis in rats." Acta Obst Gynaec Jpn. 49. S323 (1997)
Tamotsue Kiya:“催乳素诱导的大鼠结构性黄体溶解中的细胞周期依赖性细胞凋亡。”
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Yoshimitsu Kitajima: "Effects of prolactin treatment on glyceroaldehyde-3-phosphate dehydrogenase mRNA in rat corpus luteum." Jpn J Fertil Steril. 42. 319 (1997)
Yoshimitsu Kitajima:“催乳素治疗对大鼠黄体中甘油醛-3-磷酸脱氢酶 mRNA 的影响。”
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Toshiaki Endo: "Effects of estradiol and an aromatase inhibitor on progesterone production in human cultured luteal cells" Gynocdogical Endocrnology. (in press). (1998)
Toshiaki Endo:“雌二醇和芳香酶抑制剂对人类培养黄体细胞黄体酮产生的影响”妇科内分泌学。
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北島義盛: "ラット黄体のglyceralckhyde-3-phosphote dehydrogenase mRNA発現に対するprolactin投与による影響" 日本不妊学会雑誌. 42・3. 319 (1997)
北岛吉森:“催乳素给药对大鼠黄体中甘油醛-3-磷酸脱氢酶mRNA表达的影响”日本不孕协会杂志42・3.319(1997)。
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共 20 条
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财政年份:2010
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Study for the etiology of polycystic ovary using a rat model
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财政年份:2004
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The differences of mechanisms between normal luteal formation and occurrence of ovarian hyperstimulation syndrome
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批准号:14571574
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.56万
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财政年份:2002
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Study for the etiology and therapy of polycystic ovary syndrome and ovarian hyperstimulation syndrome.
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批准号:11671637
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.5万
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财政年份:1999
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负责人:ENDO Toshiaki
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依托单位:
LUTEAL REGRESSION AND PROTEINASE,APOPTOSIS,HEAT SHOCK PROTEIN
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批准号:06671670
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.41万
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财政年份:1994
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负责人:ENDO Toshiaki
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依托单位:
海外基金