Hypoxia increases cellular levels of phosphatidic acid and lysophospholipids in undifferentiated Caco-2 cells

IF 1.8 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Lipids Pub Date : 2023-01-28 DOI:10.1002/lipd.12366
Yoshibumi Shimizu, Keiko Tamiya-Koizumi, Toshihiko Tsutsumi, Mamoru Kyogashima, Reiji Kannagi, Soichiro Iwaki, Mineyoshi Aoyama, Akira Tokumura
{"title":"Hypoxia increases cellular levels of phosphatidic acid and lysophospholipids in undifferentiated Caco-2 cells","authors":"Yoshibumi Shimizu,&nbsp;Keiko Tamiya-Koizumi,&nbsp;Toshihiko Tsutsumi,&nbsp;Mamoru Kyogashima,&nbsp;Reiji Kannagi,&nbsp;Soichiro Iwaki,&nbsp;Mineyoshi Aoyama,&nbsp;Akira Tokumura","doi":"10.1002/lipd.12366","DOIUrl":null,"url":null,"abstract":"<p>Cancer cells are known to survive in a hypoxic microenvironment by altering their lipid metabolism as well as their energy metabolism. In this study, Caco-2 cells derived from human colon cancer, were found to have elevated intracellular levels of phosphatidic acid and its lysoform, lysophosphatidic acid (LPA), under hypoxic conditions. Our results suggested that the elevation of LPA in Caco-2 cells was mainly due to the combined increases in cellular levels of lysophosphatidylcholine and lysophosphatidylethanolamine by phospholipase A<sub>2</sub> and subsequent hydrolysis to LPA by lysophospholipase D. We detected the Ca<sup>2+</sup>-stimulated choline-producing activities toward exogenous lysophosphatidylcholines in whole Caco-2 cell homogenates, indicating their involvement in the LPA production in intact Caco-2 cells.</p>","PeriodicalId":18086,"journal":{"name":"Lipids","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2023-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Lipids","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/lipd.12366","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 1

Abstract

Cancer cells are known to survive in a hypoxic microenvironment by altering their lipid metabolism as well as their energy metabolism. In this study, Caco-2 cells derived from human colon cancer, were found to have elevated intracellular levels of phosphatidic acid and its lysoform, lysophosphatidic acid (LPA), under hypoxic conditions. Our results suggested that the elevation of LPA in Caco-2 cells was mainly due to the combined increases in cellular levels of lysophosphatidylcholine and lysophosphatidylethanolamine by phospholipase A2 and subsequent hydrolysis to LPA by lysophospholipase D. We detected the Ca2+-stimulated choline-producing activities toward exogenous lysophosphatidylcholines in whole Caco-2 cell homogenates, indicating their involvement in the LPA production in intact Caco-2 cells.

缺氧增加未分化Caco-2细胞中磷脂酸和溶血磷脂的细胞水平
癌细胞通过改变脂质代谢和能量代谢在低氧微环境中存活。在这项研究中,发现来自人类结肠癌的Caco-2细胞在缺氧条件下细胞内磷脂酸及其溶异构体溶血磷脂酸(LPA)水平升高。我们的研究结果表明,Caco-2细胞中LPA的升高主要是由于磷脂酶A2和溶血磷脂酰胆碱和溶血磷脂酰乙醇胺的细胞水平共同增加,随后被溶血磷脂酶d水解成LPA。我们在整个Caco-2细胞均质液中检测到Ca2+刺激的外源性溶血磷脂酰胆碱产生胆碱的活性,表明它们参与了完整Caco-2细胞中LPA的产生。
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
Lipids
Lipids 生物-生化与分子生物学
CiteScore
4.20
自引率
5.30%
发文量
33
审稿时长
4-8 weeks
期刊介绍: Lipids is a journal of the American Oil Chemists'' Society (AOCS) that focuses on publishing high-quality peer-reviewed papers and invited reviews in the general area of lipid research, including chemistry, biochemistry, clinical nutrition, and metabolism. In addition, Lipids publishes papers establishing novel methods for addressing research questions in the field of lipid research.
×
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