Abstract: Objective To explore the molecular mechanism in the formation of unstable plaques. Methods The cDNA
microarray E-MTAB-2055 was downloaded from ArrayExpress database to screen the differentially expressed genes in 24
ruptured plaques against 24 stable plaques. Functional enrichment analysis was conducted to define the biological processes
and pathways involved in disease progression. The protein-protein interaction network was constructed to identify the risk
modules with close interactions. Five pairs of carotid specimens were used to validate 3 differentially expressed genes of the
risk modules by real-time PCR. Results A total of 439 genes showed differential expression in our analysis, including 232
up-regulated and 207 down-regulated genes according to the data filter criteria. Immune-related biological processes and
pathways were greatly enriched. The protein-protein interaction network and module analysis suggested that TYROBP, VCL
and CXCR4 might play critical roles in the development of unstable plaques, and differential expressions of CXCR4 and
TYROBP in carotid plaques were confirmed by real-time PCR. Conclusion Our study shows the differential gene expression
profile, potential biological processes and signaling pathways involved in the process of plaque rupture. TYROBP may be a
new candidate disease gene in the pathogenesis of unstable plaques.