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. 2019 Jun 25;40(29):2398–2408. doi: 10.1093/eurheartj/ehz303

Figure 5.

Figure 5

JCAD deficiency attenuates vascular inflammation by acquiring an atheroprotective transcriptional program. (A–B) Gene ontology (A) and KEGG2016 pathway (B) analysis of differentially expressed genes in JCAD depleted HCAECs by RNA-seq. RNA-seq data were deposited in NCBI Gene Omnibus (http://www.ncbi.nlm.nih.gov/geo/) with the accession number of GEO: GSE102498. (C) Selected atherosclerosis-relevant genes regulated by JCAD revealed by RNA-seq. * indicates established downstream target genes of YAP/TAZ. For a whole list of differentially expressed genes, please refer to Supplementary material online, Table S7. (D) Validation of RNA-seq data by real time PCR. Select downregulated and upregulated genes were presented, n = 4. (E–F) JCAD deficiency attenuates LPS-induced vascular inflammation. JCAD+/+ (WT) and JCAD−/− (KO) primary mouse lung endothelial cells were stimulated with LPS for 6 h before monocyte (THP1) adhesion assay was performed (E, n = 6). In parallel, whole cell lysates were collected for Western blot analysis to detect protein expression of VCAM1 and ICAM1 (F, n = 4), ***P < 0.001 vs. WT, ##P < 0.01 vs WT + LPS. Log2FC, Log2 fold change; siNC, scramble control siRNA; siJCAD, JCAD siRNA; LPS, lipopolysaccharide.