UNIVERSITY OF MALTA
LIFE SCIENCE RESEARCH SEMINARS
Web: http://events.um.edu.mt/scisem/
Email: scisem@um.edu.mt
Abstract form
Title: The effect of platelet-monocyte crosstalk on the monocyte
transcriptome
Presenter: Rosienne Farrugia
Contact address: Department of Biology, Junior College, University of Malta
Tel:
Fax:
Email: rosienne.farrugia@um.edu.mt
Presentation date: 7 December 2009
Abstract
The interaction of monocytes with the vasculature is influenced by activated platelets. Plaque
rupture exposes collagens resulting in platelet activation. This signal is communicated to
monocytes by cell-cell interactions and interactions with the platelet secretome. To
characterise the ensuing changes within the monocyte, we stimulated whole-blood from 14
donors with the collagen-mimetic CRP-18 and, using whole-genome microarrays, contrasted
the resulting monocyte transcriptome with the pro-inflammatory profile induced by LPS.
Whilst we observed the expected dominant role for NF-κB in LPS-stimulated monocytes,
PPARγ was the key transcription factor implicated in the response to CRP-18. Analyses of
transcriptional changes in the transmembrane receptor repertoire and integrin signalling
pathway components showed an enrichment for the expression of these proteins in CRP-18
stimulated cells. The expression levels of a number of transmembrane proteins were
confirmed by real-time PCR and increased expression of MERTK and ENG was confirmed
by flow cytometry. Furthermore, using the PPARγ-specific antagonist GW9662, the upregulation of these 2 proteins was inhibited. These data suggest that interaction with
activated platelets is a possible physiological mechanism which primes monocytes towards
an alternative M2-like phenotype responsible for adhesion, regulation of thrombosis,
scavenging and wound repair.