Ovine interferon-tau regulates expression of endometrial receptors for estrogen and oxytocin but not progesterone.
Ovine interferon-tau regulates expression of endometrial receptors for estrogen and oxytocin but not progesterone.
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绵羊干扰素 tau 调节子宫内膜受体的雌激素和催产素表达，但不调节孕激素。
DOI：
10.1095/biolreprod53.3.732
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发表时间：
1995
影响因子：
3.6
通讯作者：
Bazer,FW
中科院分区：
文献类型：
--
作者：
Spencer,TE;Becker,WC;George,P;Mirando,MA;Ogle,TF;Bazer,FW
绵羊干扰素-T (olFN-T) 可在妊娠识别期间稳定子宫内膜黄体酮受体 (PR) 和/或抑制雌激素受体 (ER) 基因表达，从而抑制子宫内膜催产素受体 (OTR) 形成和黄体分解前列腺素 (PG) F2 的产生。本研究确定了 olFN-T 在持续暴露于黄体酮导致 PR 下调期间是否稳定子宫内膜中的 PR 表达。 20 只周期性母羊在发情周期的第 2 天（第 0 天=发情）进行双侧卵巢切除并安装子宫导管。然后，母羊被随机分配，以 2 x 2 因子排列，从第 10 天到第 14 天通过宫内注射重组 olFN-T（rolFN-T；每只母羊每天 2 x 107 抗病毒单位）或对照蛋白（6 毫克/天），并从第 2 天到第 14 天（P）每天肌内注射 20 mg 黄体酮（P）或从第 2 天开始黄体酮从第 12 天到第 14 天加 50 g 雌二醇-17p (P+ E)。所有母羊均在第 15 天进行子宫切除。接受 P+ E 的母羊的子宫内膜 PR mRNA (p< 0.01) 和蛋白质 (p< 0.03) 高于仅接受 P 的母羊。然而，与对照相比，rolFN-T 处理的母羊子宫内膜中 PR mRNA 和蛋白质的增加并不那么大（p < 0.08，处理 x 类固醇）。在单独接受 P 的母羊中，PR mRNA 和免疫反应性 PR 定位于间质和深部腺上皮，而不存在于子宫内膜腔和浅层腺上皮中。无论是否进行类固醇治疗，对照组的子宫内膜 ER mRNA (p<0.02) 和 ER 蛋白 (p<0.01) 值均高于 rolFN-T 治疗的母羊。在对照组中，ER mRNA 和免疫反应性 ER 蛋白存在于管腔和腺上皮中，并且在接受雌激素的母羊的上皮和间质中增加。相比之下，rolFN-T处理的母羊子宫内膜中的子宫内膜ER mRNA和免疫反应性ER蛋白非常低或不存在，并且雌激素不会增加子宫内膜ER mRNA和免疫反应性ER蛋白。在对照组中，用 P+ E 处理的母羊的子宫内膜 OTR 密度比单独用 P 处理的母羊更高（p < 0.09）。在 rolFN 处理的母羊中，子宫内膜 OTR 密度低于对照组（p < 0.01）。结果表明 rolFN-T 不能稳定或阻止子宫内膜中 PR mRNA 或蛋白表达的自体下调。然而，无论类固醇治疗如何，rolFN-T 确实抑制母羊子宫内膜 ER 表达和 OTR 形成。该结果支持这样的假设：oIFN-的抗黄体溶解作用是抑制子宫内膜上皮中子宫内膜ER基因的表达，从而抑制OTR的形成和黄体溶解的产生。
Ovine interferon-T (olFN-T) may stabilize endometrial progesterone receptor (PR) and/or inhibit estrogen receptor (ER) gene expression during pregnancy recognition to suppress endometrial oxytocin receptor (OTR) formation and production of luteolytic prostaglandin (PG) F2, pulses. This study determined whether or not olFN-T stabilized PR expression in the endometrium during PR down-regulation by continuous exposure to progesterone. Twenty cyclic ewes were bilaterally ovariectomized and fitted with uterine catheters on Day 2 of the estrous cycle (Day 0= estrus). Ewes were then assigned randomly to be treated, in a 2 x 2 factorial arrangement, with recombinant olFN-T (rolFN-T; 2 x 107 antiviral units per ewe per day) or control proteins (6 mg/day) by intrauterine injection from Days 10 to 14, and with daily im injections of 20 mg progesterone from Days 2 to 14 (P) or progesterone from Days 2 to 14 plus 50 g estradiol-17p from Days 12 to 14 (P+ E). All ewes were hysterectomized on Day 15. Endometrial PR mRNA (p< 0.01) and protein (p< 0.03) were higher in ewes receiving P+ E than in those receiving P alone. However, the increase in PR mRNA and protein was not as great in the endometrium of rolFN-T-treated ewes as compared to controls (p< 0.08, treatment x steroid). In ewes receiving P alone, PR mRNA and immunoreactive PR were localized to stroma and deep glandular epithelium and were not present in endometrial luminal and shallow glandular epithelium. Values for endometrial ER mRNA (p< 0.02) and ER protein (p< 0.01) were greater in controls than in rolFN-T-treated ewes regardless of steroid treatment. Among controls, ER mRNA and immunoreactive ER protein were present in the luminal and glandular epithelium and were increased in the epithelium and stroma in ewes receiving estrogen. In contrast, endometrial ER mRNA and immunoreactive ER protein were very low or absent in the endometrium of rolFN-T-treated ewes and were not increased by estrogen. Among controls, endometrial OTR density was greater (p< 0.09) in ewes treated with P+ E than in those treated with P alone. In rolFN--treated ewes, endometrial OTR density was lower (p< 0.01) than in the controls. Results indicate that rolFN-T did not stabilize or prevent autolotous down-regulation of PR mRNA or protein expression in the endometrium. However, rolFN-T did suppress endometrial ER expression and OTR formation in ewes regardless of steroid treatment. The results support the hypothesis that the antiluteolytic effects of oIFN-are to suppress endometrial ER gene expression in the endometrial epithelium, thereby inhibiting formation of OTR and production of luteolytic
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