Annexin 1 mediates the rapid anti-inflammatory effects of neutrophil-derived microparticles

Dalli, Jesmond; Norling, Lucy V.; Renshaw, Derek; Cooper, Dianne; Leung, Kit‐Yi; Perretti, Mauro

doi:10.1182/blood-2008-02-140533

Cited by 248 publications

(261 citation statements)

References 39 publications

(69 reference statements)

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“…Although a number of mechanistic details about the regulation of granulocyte migration by GCs are still unknown, a large body of data indicates that Anxa1 plays a role in this function (27,(41)(42)(43). Previously published results have demonstrated that Anxa1-KO mice show a high degree of neutrophil recruitment in a zymosan model of peritonitis, which supports its important role in migration (44).…”

Section: Discussionmentioning

confidence: 85%

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

et al. 2017

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The glucocorticoid-induced leucine zipper (GILZ) gene is a pivotal mediator of the anti-inflammatory effects of glucocorticoids (GCs) that are known to regulate the function of both adaptive and innate immunity cells. Our aim was to investigate the role of GILZ in GC-induced inhibition of neutrophil migration, as this role has not been investigated before. We found that GILZ expression was induced by dexamethasone (DEX), a synthetic GC, in neutrophils, and that it regulated migration of these cells into inflamed tissues under DEX treatment. Of note, inhibition of neutrophil migration was not observed in GILZ-knockout mice with peritonitis that were treated by DEX. This was because DEX was unable to up-regulate annexin A1 (Anxa1) expression in the absence of GILZ. Furthermore, we showed that GILZ mediates Anxa1 induction by GCs by transactivating Anxa1 expression at the promoter level via binding with the transcription factor, PU.1. The present findings shed light on the role of GILZ in the mechanism of induction of Anxa1 by GCs. As Anxa1 is an important protein for the resolution of inflammatory response, GILZ may represent a new pharmacologic target for treatment of inflammatory

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Section: Discussionmentioning

confidence: 85%

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

et al. 2017

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“…Dorsal s.c. air pouches were prepared as described in Dalli et al (23). PBS (PBS+0.01% DMSO), AnxA1 2-50 (0.5 to 500 ng/ mouse), or CR-AnxA1 2-50 (0.5 to 500 pg/mouse) were administered i.v.…”

Section: Murine Air Pouchmentioning

confidence: 99%

“…Human peripheral blood PMNs and HUVECs were isolated as in Dalli et al (23). The HUVECs were plated in 35-mm dish until confluent and then incubated with human recombinant TNF-a (10 ng/ml, 4 h; R&D Systems).…”

Section: In Vitro Flow Chambermentioning

confidence: 99%

Proresolving and Tissue-Protective Actions of Annexin A1–Based Cleavage-Resistant Peptides Are Mediated by Formyl Peptide Receptor 2/Lipoxin A4 Receptor

Dalli

Consalvo²,

Ray³

et al. 2013

The Journal of Immunology

Self Cite

109

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Endogenous mechanisms regulating the host response during inflammation resolution are critical in ensuring disposal of noxious stimuli and return to homeostasis. In this article, we engineered novel Annexin A1 (AnxA1)–based peptides, AnxA12–50, that displayed specific binding to the AnxA1 receptor (formyl peptide receptor 2/Lipoxin A4 receptor [FPR2/ALX]; IC50 ∼4 nM). Intravenous administration of AnxA12–50 markedly reduced (>60%) leukocyte adhesion to postcapillary venules in wild type and Fpr1−/−, but not Fpr2/Alx−/−, mice. Generation of a metabolically stable form of this peptide (CR-AnxA12–50), engineered by substituting a cleavage site shared by human proteinase 3 and neutrophil elastase, yielded an agonist that was resistant to neutrophil-mediated cleavage and displayed enhanced proresolving actions: accelerated resolution of self-limited inflammation and enhanced macrophage efferocytosis after sterile injury, when compared with AnxA12–50. These actions were retained with human primary leukocytes where CR-AnxA12–50 decreased neutrophil–endothelial interactions (∼25–45%), and stimulated neutrophil apoptosis and macrophage efferocytosis (∼45%). In murine cardiac ischemia/reperfusion injury, CR-AnxA12–50 elicited tissue-protective actions reducing infarct size (∼60%) and incidence of 24-h death. These results identify AnxA12–50 and CR-AnxA12–50 as FPR2/ALX agonists that harness the proresolving actions of AnxA1, and thus may represent therapeutic tools for treatment of inflammatory conditions.

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“…Plasmatic levels of LMVs have been associated with unstable plaques in asymptomatic patients with high-grade carotid stenosis [13] or with progression of diabetic retinopathy [14]. LMVs are ambivalent bioactive structures affecting both proinflammatory [15,16] and anti-inflammatory processes [17]. LMVs have been primarily ascribed procoagulant properties because of the tissue factor (TF) exposure [18,19] together with procoagulant phospholipids such as phosphatidylserine (PS).…”

Section: Introductionmentioning

confidence: 99%

A new assay to evaluate microvesicle plasmin generation capacity: validation in disease with fibrinolysis imbalance

Cointe

Souab

Bouriche³

et al. 2018

J of Extracellular Vesicle

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Among extracellular vesicles, leukocyte-derived microvesicles (LMVs) have emerged as complex vesicular structures. Primarily identified as procoagulant entities, they were more recently ascribed to plasmin generation capacity (MV-PGC). The objectives of this work were (1) to develop a new hybrid bio-assay combining the specific isolation of LMVs and measurement of their PGC, and compare its performance to the original method based on centrifugation, (2) to validate MV-PGC in septic shock, combining increased levels of LMVs and fibrinolytic imbalance. Using plasma sample spiked with LMVs featuring different levels of PGC, we demonstrated that CD15-beads specifically extracted LMVs. The MV dependency of the test was demonstrated using electron microscopy, high speed centrifugation, nanofiltration and detergent-mediated solubilization and the MV-PGC specificity using plasmin-specific inhibitors, or antibodies blocking elastase or uPA. Thanks to a reaction booster (ε-ACA), we showed that the assay was more sensitive and reproducible than the original method. Moreover, it exhibited a good repeatability, inter-operator and inter-experiment reproducibility. The new immunomagnetic bio-assay was further validated in patients with septic shock. As a result, we showed that MV-PGC values were significantly lower in septic shock patients who died compared to patients who survived, both at inclusion and 24 h later (1.4 [0.8–3.0] vs 3.1 [1.7–18] A405 × 10−3/min, p = 0.02; 1.4 [1–1.6] vs 5.2 [2.2–16] A405 × 10−3/min, p = 0.004). Interestingly, combining both MV-PGC and PAI-1 in a ratio significantly improved the predictive value of PAI-1. This strategy, a hybrid capture bioassay to specifically measure LMV-PGC using for the first time, opens new perspectives for measuring subcellular fibrinolytic potential in clinical settings with fibrinolytic imbalance.

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Annexin 1 mediates the rapid anti-inflammatory effects of neutrophil-derived microparticles

Cited by 248 publications

References 39 publications

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

Proresolving and Tissue-Protective Actions of Annexin A1–Based Cleavage-Resistant Peptides Are Mediated by Formyl Peptide Receptor 2/Lipoxin A4 Receptor

A new assay to evaluate microvesicle plasmin generation capacity: validation in disease with fibrinolysis imbalance

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