ArticleBlood2011
Endothelial cell activation by antiphospholipid antibodies is modulated by Kruppel-like transcription factors.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Andrographis restrains the progression of colorectal cancer by inhibiting the KLF3/LEMD1 axis.Functional & integrative genomics · 2026Article
- Simvastatin Restores Uteroplacental Hemodynamics and Trophoblast Function in Obstetric Antiphospholipid Syndrome in a Placenta-on-a-Chip Model.Advanced healthcare materials · 2026Article
- Antiphospholipid Syndrome: An Antibody-Mediated Disease With Emerging Therapeutic Opportunities.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Article
- Interaction of antiphospholipid antibodies with endothelial cells in antiphospholipid syndrome.Frontiers in immunology · 2024Review
- KLF4 and CD55 expression and function depend on each other.Frontiers in immunology · 2023Article
- Article
- Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome.Seminars in immunopathology · 2022Review
- Palmitic acid up regulates Gal-3 and induces insulin resistance in macrophages by mediating the balance between KLF4 and NF-κB.Experimental and therapeutic medicine · 2021Article
- Antiphospholipid syndrome.Translational research : the journal of laboratory and clinical medicine · 2020Review
- NETs in APS: Current Knowledge and Future Perspectives.Current rheumatology reports · 2020Review
- Increased Adhesive Potential of Antiphospholipid Syndrome Neutrophils Mediated by β2 Integrin Mac-1.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Effects of anti-β2GPI antibodies on VWF release from human umbilical vein endothelial cells and ADAMTS13 activity.Research and practice in thrombosis and haemostasis · 2018Article
- Krüppel-like factors and vascular wall homeostasis.Journal of molecular cell biology · 2017Review
- Activated signature of antiphospholipid syndrome neutrophils reveals potential therapeutic target.JCI insight · 2017Article
- Review
- Krüppel-like factor 4 is a transcriptional regulator of M1/M2 macrophage polarization in alcoholic liver disease.Journal of leukocyte biology · 2015Article
- Global gene expression profiling of brown to white adipose tissue transformation in sheep reveals novel transcriptional components linked to adipose remodeling.BMC genomics · 2015Article
- Reduced levels of microRNAs miR-124a and miR-150 are associated with increased proinflammatory mediator expression in Krüppel-like factor 2 (KLF2)-deficient macrophages.The Journal of biological chemistry · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Antiphospholipid syndrome is characterized by thrombosis and/or recurrent pregnancy loss in the presence of antiphospholipid antibodies (APLAs). The majority of APLAs are directed against phospholipid-binding proteins, particularly β₂-glycoprotein I (β₂GPI). Anti-β₂GPI antibodies activate endothelial cells in a β₂GPI-dependent manner through a pathway that involves NF-κB. Krüppel-like factors (KLFs) play a critical role in regulating the endothelial response to inflammatory stimuli. We hypothesized that activation of endothelial cells by APLA/anti-β₂GPI antibodies might be associated with decreased expression of KLFs, which in turn might facilitate cellular activation mediated through NF-κB. Our experimental results confirmed this hypothesis, demonstrating markedly decreased expression of KLF2 and KLF4 after incubation of cells with APLA/anti-β₂GPI antibodies. Restoration of KLF2 or KLF4 levels inhibited NF-κB transcriptional activity and blocked APLA/anti-β₂GPI-mediated endothelial activation despite NF-κB p65 phosphorylation. Chromatin immunoprecipitation analysis demonstrated that inhibition of NF-κB transcriptional activity by KLFs reflects sequestration of the cotranscriptional activator CBP/p300, making this cofactor unavailable to NF-κB. These findings suggest that the endothelial response to APLA/anti-β₂GPI antibodies reflects competition between KLFs and NF-κB for their common cofactor, CBP/p300. Taken together, these observations are the first to implicate the KLFs as novel participants in the endothelial proinflammatory response to APLA/anti-β₂GPI antibodies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.