ArticleCirculation research2012
Myeloid-specific Krüppel-like factor 2 inactivation increases macrophage and neutrophil adhesion and promotes atherosclerosis.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Genome-wide expression for diagnosis of pulmonary tuberculosis: a multicohort analysis.The Lancet. Respiratory medicine · 2016Pooled it
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- Maternal Krüppel-like factor 2 (KLF2)+ CD4 T cells promote fertility and fetal tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- KLF2 controls the apoptosis of neutrophils and is associated with disease activity of systemic lupus erythematosus.Arthritis research & therapy · 2024Article
- Novel Role of Endothelial CD45 in Regulating Endothelial-to-Mesenchymal Transition in Atherosclerosis.bioRxiv : the preprint server for biology · 2024Article
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- Kruppel-like factor 2+ CD4 T cells avert microbiota-induced intestinal inflammation.Cell reports · 2023Article
- Participation of Krüppel-like Factors in Atherogenesis.Metabolites · 2023Review
- KLF2 alleviates endothelial cell injury and inhibits the formation of THP‑1 macrophage‑derived foam cells by activating Nrf2 and enhancing autophagy.Experimental and therapeutic medicine · 2022Article
- KLF2 regulates neutrophil activation and thrombosis in cardiac hypertrophy and heart failure progression.The Journal of clinical investigation · 2022Article
- Heterozygous premature termination in zinc-finger domain of Krüppel-like factor 2 gene associates with dysregulated immunity.Frontiers in immunology · 2022Article
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- Krüppel-like Factor 2 (KLF2) in Immune Cell Migration.Vaccines · 2021Review
- A pro-inflammatory mediator USP11 enhances the stability of p53 and inhibits KLF2 in intracerebral hemorrhage.Molecular therapy. Methods & clinical development · 2021Article
- The neutrotime transcriptional signature defines a single continuum of neutrophils across biological compartments.Nature communications · 2021Article
- Safeguarding the Vasculature: Redundant Transcriptional Machinery Ensures Endothelial Protection.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
rationaleHemizygous deficiency of the transcription factor Krüppel-like factor 2 (KLF2) has been shown previously to augment atherosclerosis in hypercholesterolemic mice. However, the cell type responsible for the increased atherosclerosis due to KLF2 deficiency has not been identified. This study examined the consequence of myeloid cell-specific KLF2 inactivation in atherosclerosis. METHODS AND
resultsCell-specific knockout mice were generated by Cre/loxP recombination. Macrophages isolated from myeloid-specific Klf2 knockout (myeKlf2(-/-)) mice were similar to myeKlf2(+/+) macrophages in response to activation, polarization, and lipid accumulation. However, in comparison to myeKlf2(+/+) macrophages, myeKlf2(-/-) macrophages adhered more robustly to endothelial cells. Neutrophils from myeKlf2(-/-) mice also adhered more robustly to endothelial cells, and fewer myeKlf2(-/-) neutrophils survived in culture over a 24-hour period in comparison with myeKlf2(+/+) neutrophils. When myeKlf2(-/-) mice were mated to Ldlr(-/-) mice and then fed a high fat and high cholesterol diet, significant increase in atherosclerosis was observed in the myeKlf2(-/-)Ldlr(-/-) mice compared with myeKlf2(+/+)Ldlr(-/-) littermates. The increased atherosclerosis in myeKlf2(-/-)Ldlr(-/-) mice was associated with elevated presence of neutrophils and macrophages, with corresponding increase of myeloperoxidase as well as chlorinated and nitrosylated tyrosine epitopes in their lesion areas compared with myeKlf2(+/+)Ldlr(-/-) mice.
conclusionsThis study documents a role for myeloid KLF2 expression in modulating atherosclerosis. The increased neutrophil accumulation and atherosclerosis progression with myeloid-specific KLF2 deficiency also underscores the importance of neutrophils in promoting vascular oxidative stress and atherosclerosis. Collectively, these results suggest that elevating KLF2 expression may be a novel strategy for prevention and treatment of atherosclerosis.
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