• Home
  • Search Results
  • β4GalT1 Mediates PPARγ N-Glycosylation to Attenuate Microglia Inflammatory Activation.

β4GalT1 Mediates PPARγ N-Glycosylation to Attenuate Microglia Inflammatory Activation.

Inflammation (2018-05-03)
Xiaojuan Liu, Aihong Li, Yuanyuan Ju, Wangrui Liu, Hui Shi, Renyue Hu, Zijian Zhou, Xiaolei Sun
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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Lipopolysaccharides from Escherichia coli O111:B4, γ-irradiated, BioXtra, suitable for cell culture
Sigma-Aldrich
DL-Glyceraldehyde 3-phosphate solution, 45-55 mg/mL in H2O