ArticlePloS one2015
Pharmacological Treatment with Annexin A1 Reduces Atherosclerotic Plaque Burden in LDLR-/- Mice on Western Type Diet.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
- Annexin A1: The dawn of ischemic stroke (Review).Molecular medicine reports · 2025Review
- The Role of Thrombo-inflammation in Ischemic Stroke: Focus on the Manipulation and Clinical Application.Molecular neurobiology · 2025Review
- Specialized pro-resolving mediators in vascular inflammation and atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Mapping the cellular and molecular landscape of cardiac non-myocytes in murine diabetic cardiomyopathy.iScience · 2023Article
- Annexin-A1: The culprit or the solution?Immunology · 2022Review
- Article
- Inflammation Resolution: Implications for Atherosclerosis.Circulation research · 2022Review
- Annexins and cardiovascular diseases: Beyond membrane trafficking and repair.Frontiers in cell and developmental biology · 2022Review
- Review
- Atherosclerosis is a major human killer and non-resolving inflammation is a prime suspect.Cardiovascular research · 2021Review
- Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021Review
- Regulation of Inflammation and Oxidative Stress by Formyl Peptide Receptors in Cardiovascular Disease Progression.Life (Basel, Switzerland) · 2021Review
- Sex-dependent differences in the secretome of human endothelial cells.Biology of sex differences · 2021Article
- Pro-Resolving Mediator Annexin A1 Regulates Intracellular CaFrontiers in immunology · 2021Article
- Ac2-26 mimetic peptide of annexin A1 to treat severe COVID-19: A hypothesis.Medical hypotheses · 2020Article
- The crosstalk of ABCA1 and ANXA1: a potential mechanism for protection against atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2020Review
- Annexin-A1 deficiency exacerbates pathological remodelling of the mesenteric vasculature in insulin-resistant, but not insulin-deficient, mice.British journal of pharmacology · 2020Article
- Annexin A1 drives macrophage skewing to accelerate muscle regeneration through AMPK activation.The Journal of clinical investigation · 2020Article
- Annexin A1 as Neuroprotective Determinant for Blood-Brain Barrier Integrity in Neonatal Hypoxic-Ischemic Encephalopathy.Journal of clinical medicine · 2019Article
- G-Protein Coupled Receptor Targeting on Myeloid Cells in Atherosclerosis.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate therapeutic effects of annexin A1 (anxA1) on atherogenesis in LDLR-/- mice.
methodsHuman recombinant annexin A1 (hr-anxA1) was produced by a prokaryotic expression system, purified and analysed on phosphatidylserine (PS) binding and formyl peptide receptor (FPR) activation. Biodistribution of 99mTechnetium-hr-anxA1 was determined in C57Bl/6J mice. 12 Weeks old LDLR-/- mice were fed a Western Type Diet (WTD) during 6 weeks (Group I) or 12 weeks (Group P). Mice received hr-anxA1 (1 mg/kg) or vehicle by intraperitoneal injection 3 times per week for a period of 6 weeks starting at start of WTD (Group I) or 6 weeks after start of WTD (Group P). Total aortic plaque burden and phenotype were analyzed using immunohistochemistry.
resultsHr-anxA1 bound PS in Ca2+-dependent manner and activated FPR2/ALX. It inhibited rolling and adherence of neutrophils but not monocytes on activated endothelial cells. Half lives of circulating 99mTc-hr-anxA1 were <10 minutes and approximately 6 hours for intravenously (IV) and intraperitoneally (IP) administered hr-anxA1, respectively. Pharmacological treatment with hr-anxA1 had no significant effect on initiation of plaque formation (-33%; P = 0.21)(Group I) but significantly attenuated progression of existing plaques of aortic arch and subclavian artery (plaque size -50%, P = 0.005; necrotic core size -76% P = 0.015, hr-anxA1 vs vehicle) (Group P).
conclusionHr-anxA1 may offer pharmacological means to treat chronic atherogenesis by reducing FPR-2 dependent neutrophil rolling and adhesion to activated endothelial cells and by reducing total plaque inflammation.
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