Specific Inflammatory Stimuli Lead to Distinct Platelet Responses in mice and Humans

Different inflammatory stimuli contribute to the formation of atherosclerosis. It is hypothesized that although the end result is the same - plaque formation in arterial vessels - the pathogenesis is dependent on the etiology. In particular, platelets will respond differently depending on the inflammatory stimuli and timepoint. Using a microarray and platelet inflammatory function studies, we identified the transcriptional and functional changes that occur early and late with different inflammatory stimuli. ApoE-/- C57BL/6 mice were left untreated (control) or administered oral P. gingivalis (Pg) or intranasal C. pneumoniae (Cp) for 3 weeks, and sacrificed either 1 day (early timepoint) or 9 weeks (late timepoint) after this 3-week period. A separate group of animals was fed a Western Diet (WD) for 9 weeks and then sacrificed. Whole blood samples were collected from each animal into citrate solution and serially centrifuged to produce a pure platelet population. RNA was extracted and pooled from each experimental group and hybridized to Affymetrix Mouse Gene 1.0 ST microarrays.