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Published in: Inflammation 4/2018

01-08-2018 | ORIGINAL ARTICLE

β4GalT1 Mediates PPARγ N-Glycosylation to Attenuate Microglia Inflammatory Activation

Authors: Xiaojuan Liu, Aihong Li, Yuanyuan Ju, Wangrui Liu, Hui Shi, Renyue Hu, Zijian Zhou, Xiaolei Sun

Published in: Inflammation | Issue 4/2018

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Abstract

The inflammatory activation of microglia has double-edged effects in central nervous system (CNS) diseases. The ligand-activated transcriptional factor peroxisome proliferator-activated receptor γ (PPARγ) inhibits the inflammatory response. β-1,4-Galactosyltransferase Ι (β1, 4GalT1) mediates N-glycosylation. In this study, the N-glycosylation of PPARγ, as well as two N-linked glycosylation sites in its DNA binding domain (DBD), was identified. Disruption of both sites by site-directed mutagenesis completely abrogated the N-glycosylation of PPARγ. PPAR wild-type (WT) transfection inhibited the inflammatory activation of microglia, while the anti-inflammatory function of unglycosylated PPARγ was down-regulated. In addition, β1, 4GalT1 was shown to interact with PPARγ and to mediate PPARγ glycosylation. β1, 4GalT1 promoted PPARγ’s anti-transcription and anti-inflammatory functions. Collectively, our findings define that β-1, 4GalT1 mediated PPARγ glycosylation to attenuate the inflammatory activation of microglia, which has implications for potential therapies for CNS inflammatory diseases.
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Metadata
Title
β4GalT1 Mediates PPARγ N-Glycosylation to Attenuate Microglia Inflammatory Activation
Authors
Xiaojuan Liu
Aihong Li
Yuanyuan Ju
Wangrui Liu
Hui Shi
Renyue Hu
Zijian Zhou
Xiaolei Sun
Publication date
01-08-2018
Publisher
Springer US
Published in
Inflammation / Issue 4/2018
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-018-0789-4

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