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大鼠卵巢中的δ蛋白激酶C:雌激素调节与定位

Delta protein kinase-C in the rat ovary: estrogen regulation and localization.

作者信息

Cutler R E, Maizels E T, Hunzicker-Dunn M

机构信息

Department of Cell and Molecular Biology, Northwestern University Medical School, Chicago, Illinois 60611-8940.

出版信息

Endocrinology. 1994 Oct;135(4):1669-78. doi: 10.1210/endo.135.4.7925131.

DOI:10.1210/endo.135.4.7925131
PMID:7925131
Abstract

The present studies were undertaken to examine the cellular distribution and regulation of delta protein kinase-C (PKC) at different stages of luteal differentiation in the rat. Results from in situ hybridization studies with a delta PKC-specific probe demonstrated that delta PKC was localized specifically in granulosa cells of healthy preantral, small antral, and preovulatory follicles and corpora lutea from the second half of pregnancy. Northern and Western blot analyses showed that levels of delta PKC protein and messenger RNA were elevated 25- and 35-fold, respectively, in the second half of pregnancy over levels in preovulatory follicle-enriched ovaries, peaking between days 18-20 of pregnancy. Levels of alpha PKC, beta PKC, and zeta PKC remained unchanged during luteal differentiation. In rats hypophysectomized and hysterectomized on day 12 of pregnancy and in immature rats containing corpora lutea induced with PMSG followed by hCG injections, exogenous estrogen caused 3- and 7-fold increases in delta PKC protein, respectively. In the immature rat model, delta PKC messenger RNA levels were not altered by exogenous estrogen. Although exogenous testosterone also elevated delta PKC protein levels, exogenous dihydrotestosterone and progesterone were ineffective. These results suggest that estrogen may participate, at a posttranscriptional level, in the dramatic induction of delta PKC seen at the end of pregnancy in rat corpora lutea.

摘要

本研究旨在检测大鼠黄体分化不同阶段δ蛋白激酶C(PKC)的细胞分布及调节情况。用δ PKC特异性探针进行原位杂交研究的结果表明,δ PKC特异性定位于健康的窦前卵泡、小窦卵泡、排卵前卵泡的颗粒细胞以及妊娠后半期的黄体中。Northern印迹和Western印迹分析显示,妊娠后半期δ PKC蛋白和信使核糖核酸水平分别比富含排卵前卵泡的卵巢中的水平升高了25倍和35倍,在妊娠第18 - 20天达到峰值。在黄体分化过程中,α PKC、β PKC和ζ PKC的水平保持不变。在妊娠第12天进行垂体切除和子宫切除的大鼠以及用孕马血清促性腺激素(PMSG)诱导产生黄体后再注射人绒毛膜促性腺激素(hCG)的未成熟大鼠中,外源性雌激素分别使δ PKC蛋白增加了3倍和7倍。在未成熟大鼠模型中,外源性雌激素未改变δ PKC信使核糖核酸水平。虽然外源性睾酮也提高了δ PKC蛋白水平,但外源性二氢睾酮和孕酮则无效。这些结果表明,雌激素可能在转录后水平参与了大鼠黄体在妊娠末期出现的δ PKC的显著诱导过程。

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