Alpha-Synuclein Inhibition Promotes Erythropoiesis by Affecting Methylation Modifications of Fructose and Mannose Metabolism.

Xinrong He, Zixiang Geng, Gang Zou, Zeyu Cui, Yu Wang, Jiamin Song, Jing Zhang, Yiye Shao, Jingtao Feng, Yuncheng Wu, Te Liu, Xiaoying Zhu
{"title":"Alpha-Synuclein Inhibition Promotes Erythropoiesis by Affecting Methylation Modifications of Fructose and Mannose Metabolism.","authors":"Xinrong He, Zixiang Geng, Gang Zou, Zeyu Cui, Yu Wang, Jiamin Song, Jing Zhang, Yiye Shao, Jingtao Feng, Yuncheng Wu, Te Liu, Xiaoying Zhu","doi":"10.1089/scd.2024.0160","DOIUrl":null,"url":null,"abstract":"<p><p>Ninety-nine percent of alpha-synuclein (α-syn) in the human body is distributed in erythrocytes. However, the role that α-syn plays in erythropoiesis remains unclear. To determine the effect of α-syn on erythroid differentiation, the erythroid cells, derived from human CD34+ progenitors in the umbilical cord, were cultured in a system composed of a series of cytokines and harvested after 6 days. Our work showed α-syn inhibition-promoted erythropoiesis as characterized by altered activity of surface markers of erythroid development such as CD49d, CD36, and CD71; and different methylation status of GDP-D-mannose dehydratase, aldolase fructose-bisphosphate A, and sorbitol dehydrogenase, key enzymes involved in fructose and mannose metabolism. Reduced adenosine triphosphate and elevated lactic acid also suggested a shift in cellular metabolism from mitochondrial respiration to glycolysis. Our study revealed a previously unknown role for α-syn as a methylation regulator that alters the activity of key enzymes of the fructose and mannose metabolism, thus contributing to erythropoiesis.</p>","PeriodicalId":94214,"journal":{"name":"Stem cells and development","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Stem cells and development","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/scd.2024.0160","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Ninety-nine percent of alpha-synuclein (α-syn) in the human body is distributed in erythrocytes. However, the role that α-syn plays in erythropoiesis remains unclear. To determine the effect of α-syn on erythroid differentiation, the erythroid cells, derived from human CD34+ progenitors in the umbilical cord, were cultured in a system composed of a series of cytokines and harvested after 6 days. Our work showed α-syn inhibition-promoted erythropoiesis as characterized by altered activity of surface markers of erythroid development such as CD49d, CD36, and CD71; and different methylation status of GDP-D-mannose dehydratase, aldolase fructose-bisphosphate A, and sorbitol dehydrogenase, key enzymes involved in fructose and mannose metabolism. Reduced adenosine triphosphate and elevated lactic acid also suggested a shift in cellular metabolism from mitochondrial respiration to glycolysis. Our study revealed a previously unknown role for α-syn as a methylation regulator that alters the activity of key enzymes of the fructose and mannose metabolism, thus contributing to erythropoiesis.

人体内 99% 的α-突触核蛋白(α-syn)分布在红细胞中。然而,α-syn在红细胞生成过程中所起的作用仍不清楚。为了确定α-syn对红细胞分化的影响,我们在由一系列细胞因子组成的体系中培养了红细胞(来源于脐带中的人类CD34+祖细胞),并在6天后收获。我们的研究表明,α-syn抑制促进了红细胞生成,其特征是红细胞发育表面标志物(如CD49d、CD36和CD71)的活性发生了改变;参与果糖和甘露糖代谢的关键酶GDP-D-甘露糖脱水酶、果糖二磷酸醛缩酶A和山梨醇脱氢酶的甲基化状态也不同。三磷酸腺苷的减少和乳酸的升高也表明细胞代谢从线粒体呼吸转向了糖酵解。我们的研究揭示了α-syn作为甲基化调节因子所扮演的一个之前未知的角色,它改变了果糖和甘露糖代谢关键酶的活性,从而促进了红细胞生成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信