H3K18 lactylation-mediated nucleotide-binding oligomerization domain-2 (NOD2) expression promotes bilirubin-induced pyroptosis of astrocytes DOI Creative Commons
Jing Li, Siyu Li, Qian Sun

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: March 12, 2025

Histone lactylation, a newly glycosis-related histone modification, plays crucial role in the regulation of gene expression various immune cells. However, lactylation astrocytes remains unclear. Here, this study showed that H3K18 (H3K18la) levels were upregulated primary under unconjugated bilirubin (UCB) stimulation and hippocampus encephalopathy (BE) rats. Inhibition glycolysis decreased H3K18la attenuated pyroptosis both vitro vivo. CUT& Tag RNA-seq results revealed was enriched at promoter nucleotide-binding oligomerization domain 2 (NOD2) promoted its transcription. Moreover, NOD2 boosted activation downstream mitogen-activated protein kinase (MAPK) nuclear factor-kappa B (NF-κB) signaling pathways, which exacerbated neuroinflammation BE. Collectively, provides novel understanding epigenetic astrocytes, interruption H3K18la/NOD2 axis may represent therapeutic strategy for treating encephalopathy.

Language: Английский

H3K18 lactylation-mediated nucleotide-binding oligomerization domain-2 (NOD2) expression promotes bilirubin-induced pyroptosis of astrocytes DOI Creative Commons
Jing Li, Siyu Li, Qian Sun

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: March 12, 2025

Histone lactylation, a newly glycosis-related histone modification, plays crucial role in the regulation of gene expression various immune cells. However, lactylation astrocytes remains unclear. Here, this study showed that H3K18 (H3K18la) levels were upregulated primary under unconjugated bilirubin (UCB) stimulation and hippocampus encephalopathy (BE) rats. Inhibition glycolysis decreased H3K18la attenuated pyroptosis both vitro vivo. CUT& Tag RNA-seq results revealed was enriched at promoter nucleotide-binding oligomerization domain 2 (NOD2) promoted its transcription. Moreover, NOD2 boosted activation downstream mitogen-activated protein kinase (MAPK) nuclear factor-kappa B (NF-κB) signaling pathways, which exacerbated neuroinflammation BE. Collectively, provides novel understanding epigenetic astrocytes, interruption H3K18la/NOD2 axis may represent therapeutic strategy for treating encephalopathy.

Language: Английский

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