多组学分析显示,PRMT5调节了白色脂肪细胞中的膜运输和胆固醇合成
Xiyue Chen1, Zhihao Jia1,2, Xiashiyao Zhang3
1Department of Animal Sciences, Purdue University, West Lafayette, Indiana, USA.
概括
蛋白质氨酸甲基转移酶5 (PRMT5) 调节脂肪组织功能和全身能量平衡. 它在小鼠中的淘汰会影响葡萄糖,脂肪酸和胆固醇的新陈代谢,揭示了新型表观遗传在代谢平衡中的作用.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 脂肪组织生物学 脂肪组织生物学
背景情况:
- 脂肪组织 (AT) 对于能量恒温至关重要;其功能障碍导致代谢障碍.
- 蛋白质氨酸甲基转移酶5 (PRMT5) 已知在AT中具有致癌作用和新兴的生理功能.
- 人们对PRMT5在AT中的作用的确切机制知之甚少.
研究的目的:
- 为了研究PRMT5在脂肪组织中的生理功能.
- 阐明PRMT5在AT内的代谢调节中的作用背后的分子机制.
主要方法:
- 无偏的RNA测序和脂质组分析是在野生类型和脂肪细胞特异性淘汰 (Prmt5) 小鼠的脂肪组织上进行的.
- 采用基因表达分析和详细的脂质组成分析.
主要成果:
- 脂肪细胞中Prmt5的淘汰改变了参与新陈代谢和膜运输的基因,特别是高调葡萄糖运输/糖解基因和低调脂肪酸运输基因.
- 脂质组分析显示了三糖醇,脂肪酸和甘油脂的显著变化.
- 敲击Prmt5促进了胆固醇生物合成,导致小鼠的高脂血症和肝硬化.
结论:
- 在脂肪组织中,PRMT5作为代谢恒常的表观遗传调节剂.
- PRMT5协调膜运输,平衡葡萄糖和脂肪酸代谢,并影响胆固醇生物合成.
- PRMT5的蛋白质甲基化代表了调节系统能量平衡的新机制.
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