Butyrate drives the acetylation of histone H3K9 to activate steroidogenesis through PPARγ and PGC1α pathways in ovarian granulosa cells,The FASEB Journal

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Butyrate drives the acetylation of histone H3K9 to activate steroidogenesis through PPARγ and PGC1α pathways in ovarian granulosa cells
The FASEB Journal ( IF 4.8 ) Pub Date : 2021-01-12 , DOI: 10.1096/fj.202000444r
Qianhong Ye _{1,

2} , Xiangfang Zeng _{1,

2} , Shuai Wang _{1,

3} , Xiangzhou Zeng _{1,

2} , Guangxin Yang _{1,

2} , Changchuan Ye _{1,

2} , Shuang Cai _{1,

2} , Meixia Chen _{1,

2} , Siyu Li _{1,

2} , Shiyan Qiao _{1,

2}

Affiliation

Maintaining ovarian steroidogenesis is of critical importance, considering that steroid hormones are required for successful establishment and maintenance of pregnancy and proper development of embryos and fetuses. Investigating the mechanism that butyrate modulates the ovarian steroidogenesis is beneficial for understanding the impact of lipid nutrition on steroidogenesis. Herein, we identified that butyrate improved estradiol and progesterone synthesis in rat primary ovarian granulosa cells and human granulosa KGN cells and discovered the related mechanism. Our data indicated that butyrate was sensed by GPR41 and GPR43 in ovarian granulosa cells. Butyrate primarily upregulated the acetylation of histone H3K9 (H3K9ac). Chromatin immune-precipitation and sequencing (ChIP-seq) data of H3K9ac revealed the influenced pathways involving in the mitochondrial function (including cellular metabolism and steroidogenesis) and cellular antioxidant capacity. Additionally, increasing H3K9ac by butyrate further stimulated the PPARγ/CD36/StAR pathways to increase ovarian steroidogenesis and activated PGC1α to enhance mitochondrial dynamics and alleviate oxidative damage. The improvement in antioxidant capacity and mitochondrial dynamics by butyrate enhanced ovarian steroidogenesis. Collectively, butyrate triggers histone H3K9ac to activate steroidogenesis through PPARγ and PGC1α pathways in ovarian granulosa cells.

中文翻译：

丁酸盐驱动组蛋白 H3K9 乙酰化以通过卵巢颗粒细胞中的 PPARγ 和 PGC1α 通路激活类固醇生成

考虑到类固醇激素是成功建立和维持妊娠以及胚胎和胎儿的正常发育所必需的，因此维持卵巢类固醇生成至关重要。研究丁酸盐调节卵巢类固醇生成的机制有助于了解脂质营养对类固醇生成的影响。在此，我们确定丁酸盐改善了大鼠原代卵巢颗粒细胞和人颗粒 KGN 细胞中雌二醇和孕酮的合成，并发现了相关机制。我们的数据表明丁酸盐在卵巢颗粒细胞中被 GPR41 和 GPR43 感知。丁酸盐主要上调组蛋白 H3K9 (H3K9ac) 的乙酰化。H3K9ac 的染色质免疫沉淀和测序 (ChIP-seq) 数据揭示了涉及线粒体功能（包括细胞代谢和类固醇生成）和细胞抗氧化能力的受影响途径。此外，丁酸盐增加 H3K9ac 进一步刺激 PPARγ/CD36/StAR 通路以增加卵巢类固醇生成并激活 PGC1α 以增强线粒体动力学并减轻氧化损伤。丁酸盐对抗氧化能力和线粒体动力学的改善增强了卵巢类固醇的生成。总的来说，丁酸盐触发组蛋白 H3K9ac 通过卵巢颗粒细胞中的 PPARγ 和 PGC1α 通路激活类固醇生成。通过丁酸盐增加 H3K9ac 进一步刺激 PPARγ/CD36/StAR 通路以增加卵巢类固醇生成并激活 PGC1α 以增强线粒体动力学并减轻氧化损伤。丁酸盐对抗氧化能力和线粒体动力学的改善增强了卵巢类固醇的生成。总的来说，丁酸盐触发组蛋白 H3K9ac 通过卵巢颗粒细胞中的 PPARγ 和 PGC1α 通路激活类固醇生成。通过丁酸盐增加 H3K9ac 进一步刺激 PPARγ/CD36/StAR 通路以增加卵巢类固醇生成并激活 PGC1α 以增强线粒体动力学并减轻氧化损伤。丁酸盐对抗氧化能力和线粒体动力学的改善增强了卵巢类固醇的生成。总的来说，丁酸盐触发组蛋白 H3K9ac 通过卵巢颗粒细胞中的 PPARγ 和 PGC1α 通路激活类固醇生成。

更新日期：2021-01-12

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