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短期暴露于寒冷会在棕色脂肪中诱导持久的表观遗传记忆

Shin-Ichi Inoue¹, Matthew J Emmett², Hee-Woong Lim³

¹Institute for Diabetes, Obesity, and Metabolism, and Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.

Cell metabolism

|June 18, 2024

概括

短期暴露于寒冷会保护在棕色脂肪组织 (BAT) 中缺乏基因组脱乙酶3 (HDAC3) 的小鼠免受致命的低温. 这种保护涉及C/EBPβ依赖的表观遗传记忆,增强了热生成基因表达.

科学领域:

代谢和内分泌学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
热调节热调节热调节

背景情况:

基斯脱乙酶3 (HDAC3) 对于棕色脂肪组织 (BAT) 功能至关重要.
在BAT中HDAC3缺陷会影响热生成反应和寒冷生存.
在BAT中冷适应和记忆背后的机制尚未完全理解.

研究的目的:

调查短期轻度寒冷暴露 (STEMCT) 是否可以保护HDAC3缺乏BAT的小鼠免受低温.
阐明分子机制,包括关键的转录因子和表观遗传变化,参与这种寒冷适应.
为了确定这种保护效应的持续时间和潜在基础.

主要方法:

使用HDAC3BT淘汰 (KO) 小鼠和野生类型的 littermates.
暴露于短期温和寒冷温度 (15°C24小时) 的小鼠,随后受到急性寒冷挑战 (4°C).
评估了发热基因表达 (PGC-1α,UCP1) 和转录因子C/EBPβ的作用,使用基因删除和病毒介导的淘汰.

主要成果:

在HDAC3 BAT KO小鼠中,STEMCT对致命的低温给予了显著的保护.
保护与恢复PGC-1α和UCP1的诱导有关,这取决于这些因素.
在长达7天的时间内,观察到转录激活剂C/EBPβ的持续增加,这种冷适应性记忆独立于HDAC3.3的介导.

结论:

短期轻度寒冷暴露可以在棕色脂肪组织中建立持久的保护性记忆.
这种记忆是由一个依赖于C/EBPβ的表观遗传机制介导的,增强了热生成.
这一发现揭示了在棕色脂肪组织中适应寒冷的新型HDAC3独立途径.

关键词:

C/EBPββ 在线阅读一个错误的错误.在 HDAC3 中,HDAC3 是它们是PGC-1α.在UCP1中,UCP1是UCP1.棕色脂肪组织棕色脂肪组织寒冷的记忆是一种冷静的记忆.线粒体中的线粒体.氧化酸化是一种氧化酸化.热生成是一种热生成.

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