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肥胖患者血浆和肠道来源的细胞外囊泡的蛋白质组学分析。

Proteomic Profiling of Plasma- and Gut-Derived Extracellular Vesicles in Obesity.

机构信息

Metabolic Diseases Research Group, iNOVA4Health, NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, 1169-056 Lisboa, Portugal.

Computational and Experimental Biology Group, iNOVA4Health, NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, 1169-056 Lisboa, Portugal.

出版信息

Nutrients. 2024 Mar 4;16(5):736. doi: 10.3390/nu16050736.

DOI:10.3390/nu16050736
PMID:38474865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10935251/
Abstract

Obesity entails metabolic alterations across multiple organs, highlighting the role of inter-organ communication in its pathogenesis. Extracellular vesicles (EVs) are communication agents in physiological and pathological conditions, and although they have been associated with obesity comorbidities, their protein cargo in this context remains largely unknown. To decipher the messages encapsulated in EVs, we isolated plasma-derived EVs from a diet-induced obese murine model. Obese plasma EVs exhibited a decline in protein diversity while control EVs revealed significant enrichment in protein-folding functions, highlighting the importance of proper folding in maintaining metabolic homeostasis. Previously, we revealed that gut-derived EVs' proteome holds particular significance in obesity. Here, we compared plasma and gut EVs and identified four proteins exclusively present in the control state of both EVs, revealing the potential for a non-invasive assessment of gut health by analyzing blood-derived EVs. Given the relevance of post-translational modifications (PTMs), we observed a shift in chromatin-related proteins from glycation to acetylation in obese gut EVs, suggesting a regulatory mechanism targeting DNA transcription during obesity. This study provides valuable insights into novel roles of EVs and protein PTMs in the intricate mechanisms underlying obesity, shedding light on potential biomarkers and pathways for future research.

摘要

肥胖症涉及多个器官的代谢改变，突出了器官间通讯在其发病机制中的作用。细胞外囊泡 (EVs) 是生理和病理条件下的通讯剂，尽管它们与肥胖症的合并症有关，但它们在这种情况下的蛋白质货物在很大程度上仍然未知。为了解密 EVs 中封装的信息，我们从饮食诱导的肥胖小鼠模型中分离了血浆衍生的 EVs。肥胖症血浆 EVs 表现出蛋白质多样性下降，而对照 EVs 则显示出蛋白质折叠功能的显著富集，突出了正确折叠在维持代谢平衡中的重要性。以前，我们揭示了肠道衍生 EVs 的蛋白质组在肥胖症中具有特殊意义。在这里，我们比较了血浆和肠道 EVs，并鉴定出了仅存在于两种 EV 对照状态下的四种蛋白质，这表明通过分析血液衍生的 EVs 可以非侵入性地评估肠道健康。鉴于翻译后修饰 (PTMs) 的相关性，我们观察到肥胖症肠道 EVs 中与染色质相关的蛋白质从糖化到乙酰化的转变，表明在肥胖症期间针对 DNA 转录的调节机制。这项研究为 EV 和蛋白质 PTM 在肥胖症复杂机制中的新作用提供了有价值的见解，为未来的研究提供了潜在的生物标志物和途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/3260034b4864/nutrients-16-00736-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/5f3f239e34ab/nutrients-16-00736-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/7e8e9edfb5fb/nutrients-16-00736-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/300eefc8ad76/nutrients-16-00736-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/519195eb604f/nutrients-16-00736-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/497285601b04/nutrients-16-00736-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/3260034b4864/nutrients-16-00736-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/5f3f239e34ab/nutrients-16-00736-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/7e8e9edfb5fb/nutrients-16-00736-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/300eefc8ad76/nutrients-16-00736-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/519195eb604f/nutrients-16-00736-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/497285601b04/nutrients-16-00736-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30ce/10935251/3260034b4864/nutrients-16-00736-g006.jpg

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