Formyl-Peptide Receptor 2/3/Lipoxin A 4 Receptor Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation | Zendy

Shantel Vital | Zendy; Felix Becker | Zendy; Paul M. Holloway | Zendy; Janice Russell | Zendy; Mauro Perretti | Zendy; D. Neil Granger | Zendy; Felicity N. E. Gavins | Zendy

Open Access

Formyl-Peptide Receptor 2/3/Lipoxin A ₄ Receptor Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation

Author(s) -

Shantel Vital,

Felix Becker,

Paul M. Holloway,

Janice Russell,

Mauro Perretti,

D. Neil Granger,

Felicity N. E. Gavins

Publication year - 2016

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.115.020633

Subject(s) - lipoxin , medicine , pharmacology , inflammation , formyl peptide receptor , intravital microscopy , platelet activation , ischemia , receptor , aspirin , platelet , immunology , microcirculation , chemotaxis

Platelet activation at sites of vascular injury is essential for hemostasis, but it is also a major pathomechanism underlying ischemic injury. Because anti-inflammatory therapies limit thrombosis and antithrombotic therapies reduce vascular inflammation, we tested the therapeutic potential of 2 proresolving endogenous mediators, annexin A1 N-terminal derived peptide (AnxA1Ac2-26) and aspirin-triggered lipoxin A4 (15-epi-lipoxin A4), on the cerebral microcirculation after ischemia/reperfusion injury. Furthermore, we tested whether the lipoxin A4 receptor formyl-peptide receptor 2/3 (Fpr2/3; ortholog to human FPR2/lipoxin A4 receptor) evoked neuroprotective functions after cerebral ischemia/reperfusion injury.

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