Exposure of Bovine Granulosa Cells to Lipopolysaccharide Reduces Progesterone Secretion During Luteinization.

IF 3.1 2区 生物学 Q2 REPRODUCTIVE BIOLOGY
Zachary K Seekford, Stephanie E Wohlgemuth, I Martin Sheldon, John J Bromfield
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Abstract

Uterine disease reduces fertility in dairy cows and is caused by pathogenic bacteria. During disease, lipopolysaccharide (LPS) accumulates in follicular fluid and triggers granulosa cell inflammation via the Toll-like receptor 4 pathway. Follicle growth and plasma estradiol are reduced in cows with uterine disease, and treatment of bovine granulosa cells with LPS reduces CYP19A1 expression and estradiol synthesis. It is unclear if the effects of LPS on the steroidogenic capacity of granulosa cells persist in cells during luteinization. We hypothesized that acute exposure of granulosa cells to LPS would alter progesterone synthesis during luteinization. Here, we demonstrate that acute exposure of granulosa cells to LPS reduces progesterone synthesis during a 9-day period of luteinization after LPS treatment. We show that exposure of granulosa cells to LPS does not alter the gene expression of STAR, HSD3B1 or CYP11A1, or cellular respiration during luteinization. However, acute exposure of granulosa cells to LPS reduces the abundance of intracellular lipid, mitochondria density and cholesterol uptake during luteinization, suggesting a potential mechanism of altered steroidogenesis after acute inflammation. Collectively, these findings show that exposure of granulosa cells to LPS reduces progesterone synthesis during luteinization which is associated with altered lipid droplets and mitochondria accumulation required for steroidogenesis. Perturbations to granulosa cell physiology during uterine disease may have prolonged effects on ovarian function that contribute to reduced fertility of cows. Understanding the effects of uterine disease on corpus luteum function after disease resolution can help explain disease associated subfertility in cattle.

暴露于脂多糖的牛颗粒细胞减少黄体化过程中黄体酮的分泌。
子宫疾病降低奶牛的生育能力,是由致病菌引起的。在疾病期间,脂多糖(LPS)在卵泡液中积累,并通过toll样受体4途径引发颗粒细胞炎症。患有子宫疾病的奶牛卵泡生长和血浆雌二醇降低,用LPS处理牛颗粒细胞可降低CYP19A1表达和雌二醇合成。目前尚不清楚LPS对颗粒细胞的类固醇生成能力的影响是否在黄体化过程中持续存在。我们假设颗粒细胞急性暴露于LPS会改变黄体生成过程中黄体酮的合成。在这里,我们证明颗粒细胞急性暴露于LPS后,在LPS处理后的9天黄体化期间,黄体酮合成减少。我们发现,颗粒细胞暴露于LPS不会改变STAR、HSD3B1或CYP11A1的基因表达,也不会改变黄体化过程中的细胞呼吸。然而,颗粒细胞急性暴露于LPS会降低细胞内脂质丰度、线粒体密度和黄体生成过程中的胆固醇摄取,提示急性炎症后改变类固醇生成的潜在机制。总的来说,这些发现表明,颗粒细胞暴露于LPS会减少黄体生成过程中的黄体酮合成,这与类固醇生成所需的脂滴和线粒体积累的改变有关。子宫疾病期间对颗粒细胞生理的扰动可能对卵巢功能产生长期影响,从而导致奶牛的生育能力下降。了解疾病消退后子宫疾病对黄体功能的影响有助于解释牛疾病相关的低生育能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biology of Reproduction
Biology of Reproduction 生物-生殖生物学
CiteScore
6.30
自引率
5.60%
发文量
214
审稿时长
1 months
期刊介绍: Biology of Reproduction (BOR) is the official journal of the Society for the Study of Reproduction and publishes original research on a broad range of topics in the field of reproductive biology, as well as reviews on topics of current importance or controversy. BOR is consistently one of the most highly cited journals publishing original research in the field of reproductive biology.
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