ArticleiScience2024
Remodeling of the endothelial cell transcriptional program via paracrine and DNA-binding activities of MPO.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Myeloperoxidase promotes a tumorigenic microenvironment in non-small cell lung cancer.Redox biology · 2026Article
- Comparative analysis of myeloperoxidase deficiency in humans and mice: Conserved and species-specific effects on neutrophil biology.Redox biology · 2026Article
- Research advances in epigenetic modifications and post-translational modifications in endothelial-mesenchymal transition.Epigenetics & chromatin · 2025Review
- Establishment and application of nano-liposomes system for targeted therapy of methicillin-resistantMaterials today. Bio · 2025Article
- Endothelial-to-mesenchymal transition enhances permissiveness to AAV vectors in cardiac endothelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloperoxidase (MPO) is an enzyme that functions in host defense. MPO is released into the vascular lumen by neutrophils during inflammation and may adhere and subsequently penetrate endothelial cells (ECs) coating vascular walls. We show that MPO enters the nucleus of ECs and binds chromatin independently of its enzymatic activity. MPO drives chromatin decondensation at its binding sites and enhances condensation at neighboring regions. It binds loci relevant for endothelial-to-mesenchymal transition (EndMT) and affects the migratory potential of ECs. Finally, MPO interacts with the RNA-binding factor ILF3 thereby affecting its relative abundance between cytoplasm and nucleus. This interaction leads to change in stability of ILF3-bound transcripts. MPO-knockout mice exhibit reduced number of ECs at scar sites following myocardial infarction, indicating reduced neovascularization. In summary, we describe a non-enzymatic role for MPO in coordinating EndMT and controlling the fate of endothelial cells through direct chromatin binding and association with co-factors.
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Registered trials
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