Abstract
OBJECTIVE: To explore the mechanism underlying the progression of newly diagnosed idiopathic thrombocytopenic purpura (ITP) to its chronic or remission state using bioinformatic methods. METHODS: GSE56232 and GSE46922 gene expression profile datasets were downloaded from Gene Expression Omnibus (GEO). Differentially expressed genes were identified and characteristic genes were screened by weighted gene co-expression network analysis. These genes were used for function enrichment analysis and construction of a protein-protein interaction network. Finally, characteristic genes were verified to determine potential molecular mechanisms underlying ITP progression. RESULTS: We found that characteristic genes in the chronic ITP group were mainly involved in intracellular processes and ion binding, while characteristic genes in the remission ITP group were involved in intracellular processes and nuclear physiological activities. We identified a sub-network of characteristic genes, LMNA, JUN, PRKACG, SMC3, which may indicate the mechanism by which newly diagnosed ITP progresses to chronic. Although no meaningful signaling pathways were found, the expression of NR3C1, TPR, SMC4, PANBP2, CHD1, and U2SURP may affect ITP progression from newly diagnosed to remission. CONCLUSION: Our findings improve the understanding of the pathogenesis and progression of ITP, and may provide new directions for the development of treatment strategies.