Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage

Abstract The functions of macrophages are governed by distinct polarization phenotypes, which can be categorized as either anti-tumor/M1 type or pro-tumor/M2 type. Glycosylation is known to play a crucial role in various cellular processes, but its influence on macrophage polarization is not well-st...

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Main Authors: Xin He, Bowen Wang, Wenli Deng, Jinhua Cao, Zengqi Tan, Xiang Li, Feng Guan
Format: Article
Language:English
Published: BMC 2024-01-01
Series:Cell Communication and Signaling
Subjects:
Online Access:https://doi.org/10.1186/s12964-023-01432-6
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author Xin He
Bowen Wang
Wenli Deng
Jinhua Cao
Zengqi Tan
Xiang Li
Feng Guan
author_facet Xin He
Bowen Wang
Wenli Deng
Jinhua Cao
Zengqi Tan
Xiang Li
Feng Guan
author_sort Xin He
collection DOAJ
description Abstract The functions of macrophages are governed by distinct polarization phenotypes, which can be categorized as either anti-tumor/M1 type or pro-tumor/M2 type. Glycosylation is known to play a crucial role in various cellular processes, but its influence on macrophage polarization is not well-studied. In this study, we observed a significant decrease in bisecting GlcNAc during M0-M1 polarization, and impaired bisecting GlcNAc was found to drive M0-M1 polarization. Using a glycoproteomics strategy, we identified Lgals3bp as a specific glycoprotein carrying bisecting GlcNAc. A high level of bisecting GlcNAc modification facilitated the degradation of Lgals3bp, while a low level of bisecting GlcNAc stabilized Lgals3bp. Elevated levels of Lgals3bp promoted M1 polarization through the activation of the NF-кB pathway. Conversely, the activated NF-кB pathway significantly repressed the transcription of MGAT3, leading to reduced levels of bisecting GlcNAc modification on Lgals3bp. Overall, our study highlights the impact of glycosylation on macrophage polarization and suggests the potential of engineered macrophages via glycosylated modification. Video Abstract
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spelling doaj.art-dd3168e503f4480490cd72c04411ec0f2024-03-05T16:36:30ZengBMCCell Communication and Signaling1478-811X2024-01-0122111110.1186/s12964-023-01432-6Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophageXin He0Bowen Wang1Wenli Deng2Jinhua Cao3Zengqi Tan4Xiang Li5Feng Guan6Key Laboratory of Resource Biology and Biotechnology Western China, Ministry of Education; Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest UniversityKey Laboratory of Resource Biology and Biotechnology Western China, Ministry of Education; Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest UniversityKey Laboratory of Resource Biology and Biotechnology Western China, Ministry of Education; Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest UniversityKey Laboratory of Resource Biology and Biotechnology Western China, Ministry of Education; Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest UniversityKey Laboratory of Resource Biology and Biotechnology Western China, Ministry of Education; Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest UniversityInstitute of Hematology, School of Medicine, Northwest UniversityKey Laboratory of Resource Biology and Biotechnology Western China, Ministry of Education; Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest UniversityAbstract The functions of macrophages are governed by distinct polarization phenotypes, which can be categorized as either anti-tumor/M1 type or pro-tumor/M2 type. Glycosylation is known to play a crucial role in various cellular processes, but its influence on macrophage polarization is not well-studied. In this study, we observed a significant decrease in bisecting GlcNAc during M0-M1 polarization, and impaired bisecting GlcNAc was found to drive M0-M1 polarization. Using a glycoproteomics strategy, we identified Lgals3bp as a specific glycoprotein carrying bisecting GlcNAc. A high level of bisecting GlcNAc modification facilitated the degradation of Lgals3bp, while a low level of bisecting GlcNAc stabilized Lgals3bp. Elevated levels of Lgals3bp promoted M1 polarization through the activation of the NF-кB pathway. Conversely, the activated NF-кB pathway significantly repressed the transcription of MGAT3, leading to reduced levels of bisecting GlcNAc modification on Lgals3bp. Overall, our study highlights the impact of glycosylation on macrophage polarization and suggests the potential of engineered macrophages via glycosylated modification. Video Abstracthttps://doi.org/10.1186/s12964-023-01432-6Bisecting GlcNAcGlycosylationMacrophagePolarizationLGALS3BP
spellingShingle Xin He
Bowen Wang
Wenli Deng
Jinhua Cao
Zengqi Tan
Xiang Li
Feng Guan
Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage
Cell Communication and Signaling
Bisecting GlcNAc
Glycosylation
Macrophage
Polarization
LGALS3BP
title Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage
title_full Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage
title_fullStr Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage
title_full_unstemmed Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage
title_short Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage
title_sort impaired bisecting glcnac reprogrammed m1 polarization of macrophage
topic Bisecting GlcNAc
Glycosylation
Macrophage
Polarization
LGALS3BP
url https://doi.org/10.1186/s12964-023-01432-6
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AT jinhuacao impairedbisectingglcnacreprogrammedm1polarizationofmacrophage
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