ArticleFrontiers in pharmacology2012
Annexin A1 N-terminal derived Peptide ac2-26 exerts chemokinetic effects on human neutrophils.
Article in Frontiers in pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- The role and application prospects of ANXA1 in gastric cancer cells.Medical oncology (Northwood, London, England) · 2025Review
- Research Progress of Annexin A1 and Its Derived Peptides in the Diagnosis and Treatment of Circulatory Diseases.Immunity, inflammation and disease · 2025Review
- Annexin A1 Is Involved in the Antitumor Effects of 5-Azacytidine in Human Oral Squamous Carcinoma Cells.Cancers · 2025Article
- Autophagy and mitophagy as potential therapeutic targets in diabetic heart condition: Harnessing the power of nanotheranostics.Asian journal of pharmaceutical sciences · 2024Review
- The landscape of immune dysregulation in pediatric sepsis at a single-cell resolution.Clinical immunology (Orlando, Fla.) · 2024Article
- N-Formyl-Methionyl-Leucyl-Phenylalanine Plays a Neuroprotective and Anticonvulsant Role in Status Epilepticus Model.Cellular and molecular neurobiology · 2023Article
- Anti-Inflammatory and Pro-Resolving Actions of the N-Terminal Peptides Ac2-26, Ac2-12, and Ac9-25 of Annexin A1 on Conjunctival Goblet Cell Function.The American journal of pathology · 2023Article
- Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.International immunopharmacology · 2023Review
- Suppression of Anti-Inflammatory Mediators in Metabolic Disease May Be Driven by Overwhelming Pro-Inflammatory Drivers.Nutrients · 2022Article
- The formyl peptide receptor agonist Ac2-26 alleviates neuroinflammation in a mouse model of pneumococcal meningitis.Journal of neuroinflammation · 2020Article
- Targeting ANXA1 abrogates Treg-mediated immune suppression in triple-negative breast cancer.Journal for immunotherapy of cancer · 2020Article
- Cyclic AMP Regulates Key Features of Macrophages via PKA: Recruitment, Reprogramming and Efferocytosis.Cells · 2020Article
- Upregulation of tropomyosin alpha-4 chain in patients' saliva with oral squamous cell carcinoma as demonstrated by Phage display.Scientific reports · 2019Article
- Preservation of Post-Infarction Cardiac Structure and Function via Long-Term Oral Formyl Peptide Receptor Agonist Treatment.JACC. Basic to translational science · 2019Article
- Cardioprotective Actions of the Annexin-A1 N-Terminal Peptide, AcFrontiers in pharmacology · 2019Article
- Annexin-A1: Therapeutic Potential in Microvascular Disease.Frontiers in immunology · 2019Review
- The advantageous role of annexin A1 in cardiovascular disease.Cell adhesion & migration · 2017Review
- Annexin A1 and the Resolution of Inflammation: Modulation of Neutrophil Recruitment, Apoptosis, and Clearance.Journal of immunology research · 2016Review
- Definition of a Novel Pathway Centered on Lysophosphatidic Acid To Recruit Monocytes during the Resolution Phase of Tissue Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Human neutrophil formyl peptide receptor phosphorylation and the mucosal inflammatory response.Journal of leukocyte biology · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is postulated that peptides derived from the N-terminal region of Annexin A1, a glucocorticoid-regulated 37-kDa protein, could act as biomimetics of the parent protein. However, recent evidence, amongst which the ability to interact with distinct receptors other then that described for Annexin A1, suggest that these peptides might fulfill other functions at variance to those reported for the parent protein. Here we tested the ability of peptide Ac2-26 to induce chemotaxis of human neutrophils, showing that this peptide can elicit responses comparable to those produced by the canonical activator formyl-Met-Leu-Phe (or FMLP). However, whilst disruption of the chemical gradient abolished the FMLP response, addition of peptide Ac2-26 in the top well of the chemotaxis chamber did not affect (10 μM) or augmented (at 30 μM) the neutrophil locomotion to the bottom well, as elicited by 10 μM peptide Ac2-26. Intriguingly, the sole addition of peptide Ac2-26 in the top wells produced a marked migration of neutrophils. A similar behavior was observed when human primary monocytes were used. Thus, peptide Ac2-26 is a genuine chemokinetic agent toward human blood leukocytes. Neutralization strategies indicated that engagement of either the GPCR termed FPR1 or its cognate receptor FPR2/ALX was sufficient to sustain peptide Ac2-26 induced neutrophil migration. Similarly, application of pharmacological inhibitors showed that cell locomotion to peptide Ac2-26 was mediated primarily by the ERK, but not the JNK and p38 pathways. In conclusion, we report here novel in vitro properties for peptide Ac2-26, promoting neutrophil and monocyte chemokinesis; a process that may contribute to accelerate the resolution phase of inflammation. We postulate that the generation of Annexin A1 N-terminal peptides at the site of inflammation may expedite the egress of migrated leukocytes thus promoting the return to homeostasis.
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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.