An in vitro model of adipose tissue-associated macrophages

IF 2.1 4区 生物学 Q2 BIOLOGY Journal of Biosciences Pub Date : 2024-08-06 DOI:10.1007/s12038-024-00464-5
Karishma Bhatia, Sandhya Tiwari, Vikas Kumar Gupta, Neerav M Sapariya, Sanjeev K Upadhyay
{"title":"An in vitro model of adipose tissue-associated macrophages","authors":"Karishma Bhatia, Sandhya Tiwari, Vikas Kumar Gupta, Neerav M Sapariya, Sanjeev K Upadhyay","doi":"10.1007/s12038-024-00464-5","DOIUrl":null,"url":null,"abstract":"<p>Obesity-related chronic low-grade inflammation plays a central role in the development of insulin resistance. Macrophages are key players in adipose tissue homeostasis, and their phenotypic shift from the anti-inflammatory or alternatively activated (M2) form to the pro-inflammatory, classically activated (M1) form is a hallmark of insulin resistance. However, adipose tissue macrophages (ATMs) have been identified as a distinct subpopulation of macrophages in several recent studies. These ATMs, described as metabolically activated macrophages (MMe), differ from M1 and are primarily found in the adipose tissue of obese individuals. In our study, we developed an <i>in vitro</i> model of MMe macrophages to establish a simple and reproducible system to understand their characteristics and role in the pathophysiology of insulin resistance. We examined their characteristics such as inflammatory patterns, surface markers, and metabolic features, and compared them with M1 and M2 macrophages. We found that a cell line-based <i>in vitro</i> model effectively mirrors the characteristics of ATMs, highlighting distinct inflammatory phenotypes, metabolism, surface markers, altered lysosomal activity, and ER stress akin to macrophages <i>in vivo</i>. This model captures the subtle distinctions between MMe and M1, and can be effectively used to study several features of macrophage–adipose interactions of therapeutic importance.</p>","PeriodicalId":15171,"journal":{"name":"Journal of Biosciences","volume":null,"pages":null},"PeriodicalIF":2.1000,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biosciences","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s12038-024-00464-5","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Obesity-related chronic low-grade inflammation plays a central role in the development of insulin resistance. Macrophages are key players in adipose tissue homeostasis, and their phenotypic shift from the anti-inflammatory or alternatively activated (M2) form to the pro-inflammatory, classically activated (M1) form is a hallmark of insulin resistance. However, adipose tissue macrophages (ATMs) have been identified as a distinct subpopulation of macrophages in several recent studies. These ATMs, described as metabolically activated macrophages (MMe), differ from M1 and are primarily found in the adipose tissue of obese individuals. In our study, we developed an in vitro model of MMe macrophages to establish a simple and reproducible system to understand their characteristics and role in the pathophysiology of insulin resistance. We examined their characteristics such as inflammatory patterns, surface markers, and metabolic features, and compared them with M1 and M2 macrophages. We found that a cell line-based in vitro model effectively mirrors the characteristics of ATMs, highlighting distinct inflammatory phenotypes, metabolism, surface markers, altered lysosomal activity, and ER stress akin to macrophages in vivo. This model captures the subtle distinctions between MMe and M1, and can be effectively used to study several features of macrophage–adipose interactions of therapeutic importance.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
脂肪组织相关巨噬细胞的体外模型
与肥胖相关的慢性低度炎症在胰岛素抵抗的发展过程中起着核心作用。巨噬细胞是脂肪组织平衡的关键角色,它们的表型从抗炎或替代活化(M2)型转变为促炎、经典活化(M1)型是胰岛素抵抗的标志。然而,最近的几项研究发现,脂肪组织巨噬细胞(ATMs)是巨噬细胞的一个独特亚群。这些被称为代谢活化巨噬细胞(MMe)的 ATMs 与 M1 不同,主要存在于肥胖者的脂肪组织中。在我们的研究中,我们建立了一个 MMe 巨噬细胞的体外模型,以建立一个简单且可重复的系统来了解它们的特征及其在胰岛素抵抗的病理生理学中的作用。我们研究了它们的特征,如炎症模式、表面标志物和代谢特征,并将它们与 M1 和 M2 巨噬细胞进行了比较。我们发现,基于细胞系的体外模型有效地反映了 ATMs 的特征,突出显示了与体内巨噬细胞相似的独特炎症表型、新陈代谢、表面标志物、溶酶体活性改变和 ER 应激。该模型捕捉到了MMe和M1之间的细微差别,可有效用于研究巨噬细胞与脂肪相互作用的几个重要治疗特征。
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 去求助
来源期刊
Journal of Biosciences
Journal of Biosciences 生物-生物学
CiteScore
5.80
自引率
0.00%
发文量
83
审稿时长
3 months
期刊介绍: The Journal of Biosciences is a quarterly journal published by the Indian Academy of Sciences, Bangalore. It covers all areas of Biology and is the premier journal in the country within its scope. It is indexed in Current Contents and other standard Biological and Medical databases. The Journal of Biosciences began in 1934 as the Proceedings of the Indian Academy of Sciences (Section B). This continued until 1978 when it was split into three parts : Proceedings-Animal Sciences, Proceedings-Plant Sciences and Proceedings-Experimental Biology. Proceedings-Experimental Biology was renamed Journal of Biosciences in 1979; and in 1991, Proceedings-Animal Sciences and Proceedings-Plant Sciences merged with it.
期刊最新文献
Comparative analysis of Quercus suber L. acorns in natural and semi-natural stands: Morphology characterization, insect attacks, and chemical composition Phosphorylation mapping of laminin γ1-chain: Kinases, functional interaction sequences, and phosphorylation-interfering cancer mutations IRF9 and STAT1 as biomarkers involved in T-cell immunity in atherosclerosis Wisdom of (molecular) crowds: How a snake’s temperature-sensing superpower separates information from misinformation CDCA: Community detection in RNA-seq data using centrality-based approach
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1