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

ABSTRACT: 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 Die

ORGANISM(S): Mus musculus

SUBMITTER: Adam Gower 

PROVIDER: E-GEOD-68835 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress