Accessibility navigation


The formyl peptide fMLF primes platelet activation and augments thrombus formation

Salamah, M. F., Ravishankar, D., Vaiyapuri, R., Moraes, L. A., Patel, K., Perretti, M., Gibbins, J. M. ORCID: https://orcid.org/0000-0002-0372-5352 and Vaiyapuri, S. ORCID: https://orcid.org/0000-0002-6006-6517 (2019) The formyl peptide fMLF primes platelet activation and augments thrombus formation. Journal of Thrombosis and Haemostasis, 17 (7). pp. 1120-1133. ISSN 1538-7836

[img]
Preview
Text (Open Access) - Published Version
· Available under License Creative Commons Attribution.
· Please see our End User Agreement before downloading.

1MB
[img] Text - Accepted Version
· Restricted to Repository staff only

1MB

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1111/jth.14466

Abstract/Summary

Formyl peptide receptors (FPRs) play pivotal roles in the regulation of innate immunity and host defence. FPRs include three family members; FPR1, FPR2/ALX and FPR3. The activation of FPR1 by its high affinity ligand, N‐formyl‐methionyl‐leucyl‐phenylalanine (fMLF) (a bacterial chemoattractant peptide), triggers intracellular signalling in immune cells such as neutrophils and exacerbates inflammatory responses to accelerate the clearance of microbial infection. Notably, fMLF has been demonstrated to induce intracellular calcium mobilisation and chemotaxis in platelets that are known to play significant roles in the regulation of innate immunity and inflammatory responses. Despite a plethora of research focused on the roles of FPR1 and its ligands such as fMLF on the modulation of immune responses, their impact on the regulation of haemostasis and thrombosis remains unexplored.

Item Type:Article
Refereed:Yes
Divisions:Life Sciences > School of Biological Sciences > Biomedical Sciences
University of Reading Malaysia
Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy > Division of Pharmacology
ID Code:83494
Publisher:Wiley

Downloads

Downloads per month over past year

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation