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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. and Vaiyapuri, S. (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

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


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
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


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