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霍乱毒素对仓鼠子宫雌激素和孕激素受体的诱导作用及蜕膜化

Induction of estrogen and progesterone receptors and decidualization in the hamster uterus by cholera toxin.

作者信息

Alleva J J, Kenimer J G, Jordan A W, Lamanna C

出版信息

Endocrinology. 1983 Jun;112(6):2095-106. doi: 10.1210/endo-112-6-2095.

DOI:10.1210/endo-112-6-2095
PMID:6851940
Abstract

Cholera toxin (CT) injected ip on day 1 (day of ovulation) of the 4-day hamster estrous cycle, when circulatory progesterone is high and estrogen low, induced a massive uterine decidual reaction, a progesterone-dependent growth normally triggered by the implanting blastocyst. However, CT injected ip on day 3, when circulatory estrogen is high and progesterone low, did not induce a decidual reaction but, instead, intensified the effects of estrogen (stromal edema and stimulation of the mucosa). These cycle day effects were reproduced in one uterine horn injected intraluminally with CT, but not in the other horn of the same animal given solvent alone as a control. The intrauterine injection of CT had no effect on the concentration of serum estrogen or progesterone. The decidual reaction resulting from intrauterine injection of CT on day 1 was accompanied by increases in estrogen receptor (femtomoles per mg DNA) in both cytoplasm and nucleus. In long term ovariectomized hamsters, an ip or intrauterine injection of CT induced only histological effects of estrogen (stromal edema and mucosal mitosis) without affecting circulatory estrogen. These estrogenic effects were accompanied by increases in receptors for estrogen and progesterone in both cytoplasm and nucleus. CT injected ip into ovariectomized hamsters primed with estrogen intensified the stromal edema and mucosal mitosis and resulted in progesterone and estrogen receptor levels equal to or greater than those after the administration of CT or estrogen alone. When progesterone was included in the priming (estrogen + progesterone + CT), all receptor levels were decreased, and a massive decidual reaction resulted. Thus, the induction of estrogen receptor by CT may have been the primary event that triggered the decidual reaction. Whether CT-induced estrogen receptor is mediated by cAMP, a known mediator of CT, remains to be determined.

摘要

在4天的仓鼠动情周期的第1天(排卵日)腹腔注射霍乱毒素(CT),此时循环中的孕酮水平高而雌激素水平低,可诱导大量子宫蜕膜反应,这是一种通常由植入的胚泡触发的孕酮依赖性生长。然而,在第3天腹腔注射CT,此时循环中的雌激素水平高而孕酮水平低,并未诱导蜕膜反应,而是增强了雌激素的作用(基质水肿和黏膜刺激)。这些周期日效应在用CT腔内注射的一个子宫角中重现,但在同一动物的另一个仅给予溶剂作为对照的子宫角中未出现。子宫内注射CT对血清雌激素或孕酮浓度没有影响。第1天子宫内注射CT导致的蜕膜反应伴随着细胞质和细胞核中雌激素受体(每毫克DNA飞摩尔)的增加。在长期卵巢切除的仓鼠中,腹腔或子宫内注射CT仅诱导雌激素的组织学效应(基质水肿和黏膜有丝分裂),而不影响循环中的雌激素。这些雌激素效应伴随着细胞质和细胞核中雌激素和孕酮受体的增加。对用雌激素预处理的卵巢切除仓鼠腹腔注射CT会增强基质水肿和黏膜有丝分裂,并导致孕酮和雌激素受体水平等于或高于单独给予CT或雌激素后的水平。当预处理中包含孕酮(雌激素+孕酮+CT)时,所有受体水平均降低,并导致大量蜕膜反应。因此,CT诱导雌激素受体可能是触发蜕膜反应的主要事件。CT诱导的雌激素受体是否由CT的已知介质环磷酸腺苷介导,仍有待确定。

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引用本文的文献

1
Characterization of uterine growth response to cholera toxin in hamsters and test of heat-labile enterotoxin from Escherichia coli.仓鼠子宫对霍乱毒素生长反应的特征及大肠杆菌不耐热肠毒素的检测
J Clin Microbiol. 1984 Sep;20(3):506-8. doi: 10.1128/jcm.20.3.506-508.1984.