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Fig. 6 | Acta Neuropathologica Communications

Fig. 6

From: Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations

Fig. 6

Functional interaction networks of differentially expressed genes (DEGs) in lesional neurovascular units excluding in vitro brain microvascular endothelial cell (BMEC) and in vitro (BMECs). a The functional interaction network analysis of the 1225 DEGs (fold change |FC| ≥ 2; p < 0.05, false discovery rate (FDR) corrected) identified as common between in vivo and in vitro and not in the in vitro BMECs, showed six highly connected genes (with more than 50 edges) including CDK1, DLG4, GNG4, GNG7, PRKACB and GNGT2, and 50 DEGs with 31–50 edges. b The functional interaction network analysis with linkage genes of the 121 DEGs (|FC| ≥ 2; p < 0.05, FDR corrected) identified in the in vitro BMECs showed 6 DEGs with 11–30 edges including KIT, SYK, FAS, CXCR4, GNG2, LCP2, and CD247. Furthermore, nine DEGs were identified with 5 to 10 edges: PTPRJ, COL7A, SPRY, IRF8, CFTR, NOS2, TIMP1, F2RL2 and GNG5. Genes with 31–50 edges were linkage genes and included JUN, STAT3, MAPK1, EP300, UBC and SRC. The human homologous genes corresponding to the DEGs identified in each mouse models were used for the network analysis

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