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Final Program


Final Congress Guide

Biomedical Sciences

100 Section - Ogt-mediated O-GlcNAcylation promotes microglial lipophagy through modulating OGT-BRG1-ATF3-LC3 positive feedback loop following ischemic stroke

Wednesday, May 20, 2026
6:00 PM - 7:30 PM PT

    Presenting Author/Autor expositor(s)

  • CD

    Chengwei Duan, PhD

    Postgraduate
    Nantong First People's Hospital affiliated to Southeast University
    Nantong, Jiangsu, China (People's Republic)

    • Co-Author/Coautor(s)

  • WC

    Weiguan Chen, MD

    Director of Department of Rehabilitation Medicine
    Nantong First People's Hospital affiliated to Southeast University
    Nantong, Jiangsu, China (People's Republic)

    • Corresponding Author/Autor a quien dirigir la corr(s)

  • HL

    Hongjian Lu, PhD

    Professor
    Nantong First People's Hospital affiliated to Southeast University
    Nantong, Jiangsu, China (People's Republic)

Objectives :

Microglia lipophagy plays a vital role in the neuroinflammatory and neurological recovery process, but its underlying mechanism remains poorly understood in ischemic stroke. Recent research has also revealed that Ogt-mediated O-GlcNAcylation significantly regulates neuroinflammatory responses. However, the specific molecular mechanisms of how O-GlcNAcylation influences neurological recovery by regulating microglial lipophagy in the ischemic stroke remain to be elucidated.

Design:

MCAO model construction with Cx3Cr1-Cre: Ogtf/f mice.  Cx3Cr1-Cre: Ogtf/f mice after stroke, the corner experiment, the water maze experiment, and the new object recognition experiment were used to detect behavioral changes; immunofluorescence and western blot were used to detect microglial lipophagy and neuronal apoptosis. The mass spectrometry method and protein immunoprecipitation demonstrated O-GlcNAcylation alteration between ATF3 and Brg1, as well as that OGT-ATF2-Bg1 can form a complex. Nuclear cytoplasmic separation and immunofluorescence demonstrated an increase in nuclear localization following ATF3 glycosylation alteration. ATF3 and Brg1 knockdown prevent microglia lipophagy. LC3 and OGT genes are downstream target genes of ATF3, according to ChIP and PCR detection.

Results:

Following MCAO, O-GlcNAcylation expression rises and microglia lipophagy declines.  Cx3Cr1-Cre: Ogtf/f mice following MCAO improved neurological function recovery, microglial lipophagy, and decreased cerebral infarction area. ATF3 and Brg1 exist in O-GlcNAcylation. In addition, OGT-ATF2-Brg1 can form a complex. The O-GlcNAcylation promotes nuclear localization of ATF3. Microglia lipophagy is inhibited by ATF3 or Brg1 knockdown. LC3 and OGT are downstream target genes of ATF3, according to ChIP and PCR detection.

Conclusion:

OGT-mediated O-GlcNAcylation promotes microglial lipophagy through modulating the OGT-BRG1-ATF3-LC3 positive feedback loop following ischemic stroke.