TGF-beta 1 suppresses de novo cholesterol biosynthesis in granulosa-lutein cells by down-regulating DHCR24 expression via the GSK-3 beta/EZH2/H3K27me3 signaling pathway
文献类型: 外文期刊
第一作者: Li, Hui
作者: Li, Hui;Zhao, Fang;Zhao, Weimin;Chen, Fang;Fu, Yanfeng;Li, Bixia;Cheng, Jinhua;Shen, Jie;Deng, Yanfei;Ma, Shinan
作者机构:
关键词: TGF-01; DHCR24; De novo cholesterol biosynthesis
期刊名称:INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES ( 影响因子:8.2; 五年影响因子:7.8 )
ISSN: 0141-8130
年卷期: 2023 年 224 卷
页码:
收录情况: SCI
摘要: Cholesterol is a precursor to steroid hormones and can be obtained from serum LDL or de novo synthesis in steroidogenic cells. Before luteinizing hormone (LH) surge-induced ovulation, follicles remain avascular, and cholesterol required for progesterone production in granulosa cells (GCs) is derived from de novo biosynthesis. Previous studies have verified that the intrafollicular TGF-01 plays inhibitory roles in GCs luteinization, vascularization, and progesterone production. Nevertheless, the regulatory function of TGF-01 on de novo cholesterol synthesis in granulosa-lutein (GL) cells remains largely unknown. We aim to investigate this aspect in this study using in vivo cultured human GL cells. Our results suggested that TGF-01 significantly suppresses intracellular cholesterol levels and down-regulates the expression of the final step enzyme, DHCR24, that cat-alyzes de novo cholesterol synthesis. We used specific inhibitors and siRNA-mediated knockdown approaches demonstrate that TGF-01 suppression of DHCR24 expression in GL cells is mediated by the GSK-30/EZH2/ H3K27me3 signaling pathway. Further ChIP assays revealed that elevated H3K27me3 levels in the promoter region of DHCR24 play a vital role in TGF-01-induced DHCR24 down-regulation, and RNA-sequencing results confirmed these findings. Notably, our study provides a novel insight into the molecular mechanisms by which TGF-01 suppresses de novo cholesterol biosynthesis in GL cells.
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