Annexin 1 and its bioactive peptide inhibit neutrophil-endothelium interactions under flow: indication of distinct receptor involvement.
@article{Hayhoe2006Annexin1A,
title={Annexin 1 and its bioactive peptide inhibit neutrophil-endothelium interactions under flow: indication of distinct receptor involvement.},
author={Richard P. G. Hayhoe and Ahmad M. Kamal and Egle Solito and Roderick John Flower and Dianne Cooper and Mauro Perretti},
journal={Blood},
year={2006},
volume={107 5},
pages={
2123-30
}
}We have tested the effects of annexin 1 (ANXA1) and its N-terminal peptide Ac2-26 on polymorphonuclear leukocyte (PMN) recruitment under flow. Differential effects of the full-length protein and its peptide were observed; ANXA1 inhibited firm adhesion of human PMNs, while Ac2-26 significantly attenuated capture and rolling without effect on firm adhesion. Analysis of the effects of ANXA1 and Ac2-26 on PMN adhesion molecule expression supported the flow chamber results, with Ac2-26 but not ANXA1…
216 Citations
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- Biology, MedicineBlood
- 2008
PMN-derived microparticles contain functionally active AnxA1 that confers them anti-inflammatory properties; generation of thesemicroparticles in the microcirculation could promote inflammatory resolution by time-dependent dampening of cell recruitment.
neutrophil-derived microparticles Annexin 1 mediates the rapid anti-inflammatory effects of
- Biology
- 2013
It is concluded that PMN-derived microparticles contain functionally active AnxA1 that confers them anti-inflammatory properties; generation of thesemicroparticles in the microcirculation could promote inflammatory resolution by time-dependent dampening of cell recruitment.
Annexin A1 N-Terminal Derived Peptide Ac2-26 Exerts Chemokinetic Effects on Human Neutrophils
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Novel in vitro properties for peptide Ac2-26 are reported, promoting neutrophil and monocyte chemokinesis; a process that may contribute to accelerate the resolution phase of inflammation.
Functional and ultrastructural analysis of annexin A1 and its receptor in extravasating neutrophils during acute inflammation.
- BiologyThe American journal of pathology
- 2009
In vivo support is provided to the hypothesis that endogenous AnxA1 is an essential effector of endogenous anti-inflammation and an ultrastructural indication that this mediator interacts with Fpr2 in murine neutrophils is provided.
Glucocorticoid upregulation of the annexin-A1 receptor in leukocytes.
- BiologyBiochemical and biophysical research communications
- 2006
Expression of annexin-1 in equine leucocytes and the effects of the N-terminal annexin-1 peptide, Ac2-26, on equine neutrophil superoxide production.
- Biology, MedicineVeterinary immunology and immunopathology
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A novel AnxA1-dependent mechanism behind the inhibitory properties of estrogen on PMN activation is unveiled, describing a novel phenotype with a conceivable impact on the vasculoprotective effects of this hormone.
Annexin I Regulates SKCO-15 Cell Invasion by Signaling through Formyl Peptide Receptors*
- BiologyJournal of Biological Chemistry
- 2006
The findings in this study suggest that activation of nFPRs stimulates epithelial cell motility important in the development of metastasis as well as wound healing and support an autocrine/paracrine role for membrane AnxA1 in stimulating SKCO-15 cell migration through nF PR activation.
Characterizing the anti-inflammatory and tissue protective actions of a novel Annexin A1 peptide
- BiologyPloS one
- 2017
These findings identify CR-AnxA12-48 as a new ALX agonist that regulates phagocyte responses and displays tissue-protective actions.
Anti-Inflammatory Role of the Murine Formyl-Peptide Receptor 2: Ligand-Specific Effects on Leukocyte Responses and Experimental Inflammation
- BiologyThe Journal of Immunology
- 2010
The creation of a novel mouse colony in which the murine FprL1 FPR2 homologue, Fpr2, has been deleted is reported and its use to explore the biology of this receptor is described, concluding that Fpr 2 is an anti-inflammatory receptor that serves varied regulatory functions during the host defense response.
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