乙酰组分析为了解慢性间歇性缺氧对下丘脑依赖性内分泌代谢损伤的影响提供了新见解

Biology Pub Date : 2024-07-24 DOI:10.3390/biology13080559
Yaru Kong, Jie Ji, Xiaojun Zhan, Weiheng Yan, Fan Liu, Pengfei Ye, Shan Wang, Jun Tai
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引用次数: 0

摘要

小儿阻塞性睡眠呼吸暂停(OSA)是一种高发的睡眠障碍,会导致慢性间歇性缺氧(CIH),并与新陈代谢和内分泌损伤有关。蛋白质乙酰化是一种经常发生的翻译后修饰,在调节下丘脑过程中起着关键作用。然而,人们对 CIH 诱导的全局蛋白乙酰化对下丘脑功能和内分泌代谢的影响仍然知之甚少。为了弥补这一知识空白,我们进行了一项研究,利用液相色谱-质谱法分析了暴露于3周间歇性缺氧(作为CIH模型)的健康婴幼儿小鼠与正常缺氧小鼠(作为对照组)的下丘脑赖氨酸乙酰化组和蛋白质组。我们的分析确定并量化了 2453 个蛋白质中的 2699 个 Kac 位点。这些乙酰化蛋白质主要在内分泌代谢、柠檬酸循环(TCA 循环)、突触功能和昼夜节律调节方面表现出紊乱。此外,我们还观察到已知参与内分泌激素分泌的蛋白质出现了明显的下调。本研究旨在阐明 CIH 诱导下丘脑内蛋白质乙酰化改变的分子机制。通过深入了解与 CIH 相关的病理生理过程及其对下丘脑功能的影响,我们的研究结果有助于加深对 CIH 诱导的下丘脑内蛋白质乙酰化变化的后果及其在内分泌损伤中的潜在作用的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acetylome Analyses Provide New Insights into the Effect of Chronic Intermittent Hypoxia on Hypothalamus-Dependent Endocrine Metabolism Impairment
Paediatric obstructive sleep apnoea (OSA) is a highly prevalent sleep disorder resulting in chronic intermittent hypoxia (CIH) that has been linked to metabolism and endocrine impairment. Protein acetylation, which is a frequently occurring posttranslational modification, plays pivotal roles in the regulation of hypothalamic processes. However, the effects of CIH-induced global protein acetylation on hypothalamic function and endocrine metabolism remain poorly understood. To bridge this knowledge gap, we conducted a study utilizing liquid chromatography–mass spectrometry to analyse the lysine acetylome and proteome of the hypothalamus in healthy infantile mice exposed to 3 weeks of intermittent hypoxia (as a CIH model) compared to normoxic mice (as controls). Our analysis identified and quantified 2699 Kac sites in 2453 proteins. These acetylated proteins exhibited disruptions primarily in endocrine metabolism, the citrate cycle (TCA cycle), synapse function, and circadian entrainment. Additionally, we observed significant down-regulation of proteins that are known to be involved in endocrine hormone secretion. This study aimed to elucidate the molecular mechanisms underlying CIH-induced alterations in protein acetylation within the hypothalamus. By providing valuable insights into the pathophysiological processes associated with CIH and their impacts on hypothalamic function, our findings contribute to a deeper understanding of the consequences stemming from CIH-induced changes in protein acetylation within the hypothalamus as well as its potential role in endocrine impairment.
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