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Histone lactylation drives N5-methylcytosine (m5C) RNA modification via NSUN2, promoting choroidal neovascularization (CNV). Inhibiting NSUN2 in endothelial cells reduced CNV progression and vascular leakage in mice.

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Area of Science:

  • Molecular Biology
  • Epigenetics
  • Ophthalmology

Background:

  • N5-methylcytosine (m5C) is a key RNA modification impacting cellular processes.
  • The role of m5C and the NSUN2 methylase in choroidal neovascularization (CNV) is not fully understood.

Purpose of the Study:

  • To investigate the mechanism linking histone lactylation, NSUN2, m5C modification, and CNV pathogenesis.
  • To explore potential therapeutic targets for CNV.

Main Methods:

  • Analysis of NSUN2 expression and m5C levels in normal and CNV endothelial cells (ECs).
  • Investigating the effect of lactate-mediated histone lactylation on the NSUN2 promoter.
  • Utilizing NSUN2 silencing and EC-specific knockout mice (Nsun2 -/-) to assess CNV progression.
  • Employing multiomics analyses to identify downstream targets of NSUN2.

Main Results:

  • NSUN2 expression and m5C levels were elevated in CNV-ECs, correlated with increased histone lactylation.
  • NSUN2 silencing impaired EC proliferation, migration, and tube formation.
  • EC-specific Nsun2-deficient mice showed reduced retinal vascular leakage.
  • NSUN2 was found to increase m5C levels in AKAP2, activating the PKA-VEGFR2 pathway.

Conclusions:

  • Histone lactylation promotes NSUN2-mediated m5C modification, driving CNV development.
  • The NSUN2-m5C-AKAP2-PKA-VEGFR2 axis is a critical pathway in CNV pathogenesis.
  • Targeting the interplay between histone lactylation and m5C RNA modification offers a novel therapeutic strategy for CNV.