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
复制标题
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:
影响因子:
--
通讯作者:
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
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.