Annexin A1 N-terminal derived Peptide ac2-26 exerts chemokinetic effects on human neutrophils

Dalli, J., Montero-Melendez, T., McArthur, S. and Perretti, M. 2012. Annexin A1 N-terminal derived Peptide ac2-26 exerts chemokinetic effects on human neutrophils. Frontiers in Pharmacology. 3, p. 28.

TitleAnnexin A1 N-terminal derived Peptide ac2-26 exerts chemokinetic effects on human neutrophils
AuthorsDalli, J., Montero-Melendez, T., McArthur, S. and Perretti, M.
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.

JournalFrontiers in Pharmacology
Journal citation3, p. 28
ISSN1663-9812
Year2012
PublisherFrontiers Research Foundation
Publisher's versionFrontiers in Pharmacology 2012.pdf
Digital Object Identifier (DOI)doi:10.3389/fphar.2012.00028
Publication dates
Published28 Feb 2012
LicenseCC BY-NC 3.0

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Endogenous lipid- and peptide-derived anti-inflammatory pathways generated with glucocorticoid and aspirin treatment activate the lipoxin A4 receptor
Perretti, M., Chiang, N., La, M., Fierro, I.M., Marullo, S., Getting, S.J., Solito, E. and Serhan, C.N. 2002. Endogenous lipid- and peptide-derived anti-inflammatory pathways generated with glucocorticoid and aspirin treatment activate the lipoxin A4 receptor. Nature Medicine. 8 (11), pp. 1296-1302.

Activation of melanocortin type 3 receptor as a molecular mechanism for adrenocorticotropic hormone efficacy in gouty arthritis
Getting, S.J., Christian, H.C., Flower, R.J. and Perretti, M. 2002. Activation of melanocortin type 3 receptor as a molecular mechanism for adrenocorticotropic hormone efficacy in gouty arthritis. Arthritis & Rheumatism. 46 (10), pp. 2765-2775.

A novel control mechanism based on GDNF modulation of somatostatin release from sensory neurones
Malcangio, M., Getting, S.J., Grist, J., Cunningham, J.R., Bradbury, E.J., Issa, P.C., Lever, I.J., Pezet, S. and Perretti, M. 2002. A novel control mechanism based on GDNF modulation of somatostatin release from sensory neurones. FASEB Journal. 16 (7), pp. 730-732.

Characterization of CXC and CC chemokine expression in a murine model of chronic granuloma
Carollo, M., Getting, S.J., Delaney, S., Christie, M.I. and Perretti, M. 2002. Characterization of CXC and CC chemokine expression in a murine model of chronic granuloma. Inflammation Research. 51 (2), pp. 110-111.

Involvement of the receptor for formylated peptides in the in vivo anti-migratory actions of annexin 1 and its mimetics
Perretti, M., Getting, S.J., Solito, E., Murphy, P.M. and Gao, J.L. 2001. Involvement of the receptor for formylated peptides in the in vivo anti-migratory actions of annexin 1 and its mimetics. American Journal of Pathology. 158 (6), pp. 1969-1973.

Anti-inflammatory effects of a novel, potent inhibitor of poly (ADP-ribose) polymerase
Mabley, J.G., Jagtap, P., Perretti, M., Getting, S.J., Salzman, A.L., Virag, L., Szabo, E., Soriano, F.G., Liaudet, L., Hasko, G., Marton, A., Southan, G.J., Abdelkarim, G.E. and Szabo, C. 2001. Anti-inflammatory effects of a novel, potent inhibitor of poly (ADP-ribose) polymerase. Inflammation Research. 50 (11), pp. 561-569.

Arthritic diseases: melanocortin type 3 receptor agonists as potential therapeutics
Getting, S.J. and Perretti, M. 2001. Arthritic diseases: melanocortin type 3 receptor agonists as potential therapeutics. Current opinion in investigational drugs. 2 (8), pp. 1064-1069.

Natural and synthetic agonists of the melanocortin receptor type 3 possess anti-inflammatory properties
Getting, S.J., Allcock, G.H., Flower, R.J. and Perretti, M. 2001. Natural and synthetic agonists of the melanocortin receptor type 3 possess anti-inflammatory properties. Journal of Leukocyte Biology. 69 (1), pp. 98-104.

MC3-R as a novel target for anti-inflammatory therapy
Getting, S.J. and Perretti, M. 2000. MC3-R as a novel target for anti-inflammatory therapy. Drug News & Perspectives. 13 (1), pp. 19-27.

POMC gene-derived peptides activate melanocortin type 3 receptor on murine macrophages, suppress cytokine release, and inhibit neutrophil migration in acute experimental inflammation
Getting, S.J., Gibbs, L., Clark, A.J.L., Flower, R.J. and Perretti, M. 1999. POMC gene-derived peptides activate melanocortin type 3 receptor on murine macrophages, suppress cytokine release, and inhibit neutrophil migration in acute experimental inflammation. Journal of Immunology. 162 (12), pp. 7446-7453.

Compounds for use in the treatment of inflammation
Flower, R.J., Getting, S.J. and Perretti, M. 1998. Compounds for use in the treatment of inflammation.

Inhibition of poly (ADP-ribose) synthetase attenuates neutrophil recruitment and exerts anti-inflammatory effects
Szabo, C., Lim, L.H.K., Cuzzocrea, S., Getting, S.J., Zingarelli, B., Flower, R.J., Salzman, A.L. and Perretti, M. 1997. Inhibition of poly (ADP-ribose) synthetase attenuates neutrophil recruitment and exerts anti-inflammatory effects. Journal of experimental medicine. 186 (7), pp. 1041-1049.

Molecular determinants of monosodium urate crystal-induced murine peritonitis: a role for endogenous mast cells and a distinct requirement for endothelial-derived selectins
Getting, S.J., Flower, R.J., Parente, L., de Medicis, R., Lussier, A., Woliztky, B.A., Martins, M.A. and Perretti, M. 1997. Molecular determinants of monosodium urate crystal-induced murine peritonitis: a role for endogenous mast cells and a distinct requirement for endothelial-derived selectins. Journal of Pharmacology and Experimental Therapeutics. 283 (1), pp. 123-130.

Inhibition of neutrophil and monocyte recruitment by endogenous and exogenous lipocortin 1
Getting, S.J., Flower, R.J. and Perretti, M. 1997. Inhibition of neutrophil and monocyte recruitment by endogenous and exogenous lipocortin 1. British Journal of Pharmacology. 120 (6), pp. 1075-1082.

Sub-acute treatment of rats with dexamethasone reduces ICAM-1 levels on circulating monocytes
Tailor, A., Das, A.M., Getting, S.J., Flower, R.J. and Perretti, M. 1997. Sub-acute treatment of rats with dexamethasone reduces ICAM-1 levels on circulating monocytes. Biochemical and Biophysical Research Communications. 231 (3), pp. 675-678.

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