Luteoprotective roles of luteinizing hormone are mediated by not only progesterone production but also glucocorticoid conversion in bovine corpus luteum

Luteoprotective roles of luteinizing hormone are mediated by not only progesterone production but also glucocorticoid conversion in bovine corpus luteum
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黄体生成素的黄体保护作用不仅由黄体酮的产生介导,还由牛黄体中糖皮质激素的转化介导

DOI:
10.1002/mrd.22150
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发表时间:
2013
期刊:
Mol. Reprod. Dev.
影响因子:
--
通讯作者:
Kawaguchi S
Kawaguchi S
中科院分区:
--
文献类型:
--
作者:
CHEN H;ZHAU J;CHU G;KITO G,YAMAUCHI N;SHIGEYOSHI Y,HASHIMOTO S;HATTORI M-A;Kawaguchi S

文献摘要

相似文献

黄体生成素(LH)是黄体(CL)功能的关键调节因子,但其维持黄体功能的黄体保护机制尚不清楚。目前的研究探讨了黄体生成素是否能增加细胞活力并诱导皮质醇转化,以及黄体保护作用是否通过刺激局部孕酮(P4)和/或皮质醇的产生和作用来实现。在黄体中期(发情周期第8-12天)获得培养的牛黄体细胞,用黄体生成素(10 ng/ml)处理24 小时,加或不加奥那普司酮(OP,P4受体特异性拮抗剂;100 µM)、可的松(1 µM)和氨基谷氨酸亚胺(AGT,细胞色素P450侧链切割的特异性抑制剂;100 µM)。黄体生成素可显著增加11β-羟基类固醇脱氢酶(HSD11B)1mRNA和蛋白的表达,但不影响HSD11B2mRNA和蛋白的表达。这些处理还显著提高了HSD11B1的活性。黄体生成素单独作用或黄体生成素与可的松和OP联合应用均能显著提高细胞存活率。与单独使用黄体生成素相比,黄体生成素与OP或AGT联合应用可显著降低细胞存活率。总体而言,结果表明,黄体生成素不仅刺激P4的产生,还刺激HSD11B1的表达,从而增加牛CL中皮质醇的浓度,并且黄体生成素通过这些生存途径防止细胞死亡。因此,黄体生成素可能在黄体期支持黄体功能。摩尔。是Reprod。戴夫。2013年80:204-211。©2013 Wiley期刊,Inc.
Luteinizing hormone (LH) is known as a key regulator of corpus luteum (CL) function, but the luteoprotective mechanisms of LH in the maintenance of bovine CL function are not well understood. The current study investigated if LH increases cell viability and induces cortisol conversion, and if the luteoprotective action of LH is mediated by stimulating the local production and action of progesterone (P4) and/or cortisol. Cultured bovine luteal cells obtained at the mid‐luteal stage (Days 8–12 of the estrous cycle) were treated for 24 hr with LH (10 ng/ml) with/without onapristone (OP, a specific P4 receptor antagonist; 100 µM), cortisone (1 µM), and aminoglutethimide (AGT, a specific inhibitor of cytochrome P450 side‐chain cleavage; 100 µM). LH with and without OP significantly increased the mRNA and protein expressions of 11β‐hydroxysteroid dehydrogenase (HSD11B) 1, but did not affect the mRNA or protein expression ofHSD11B2. These treatments also significantly increased HSD11B1 activity. Cell viability was significantly increased by LH alone or by LH in combination with cortisone and OP. LH in combination with OP or AGT significantly decreased cell viability as compared to LH alone. The overall results suggest that LH stimulates not only P4 production but alsoHSD11B1expression, thereby increasing the cortisol concentration in the bovine CL, and that LH prevents cell death through these survival pathways. LH may consequently support CL function during the luteal phase in cattle. Mol. Reprod. Dev. 80: 204–211, 2013. © 2013 Wiley Periodicals, Inc.