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. 2021 Apr 28;118(5):1262–1275. doi: 10.1093/cvr/cvab148

Figure 2.

Figure 2

EC-specific Zeb2-KO alters expression of genes related to LSEC capillarization and HSC communication. (A) Number of differentially expressed genes in LSECs, HSCs, KCs, and HEPs (n = 2). (B) Pathways affected by Zeb2 (based on Enrichr analysis; n = 2; top). Expression of LSEC markers (determined by qRT-PCR on an extended set of mice; n = 5–7; middle) and continuous EC markers (heat map generated from the RNA sequencing dataset; n = 2; bottom). (C) NicheNet-based predictions of ligands downregulated in LSEC source cells and targets downregulated in HSC target cells (n = 2; middle). Expression of LSEC-derived ligand genes (bottom) and HSC target genes (top; highlighted in red in the middle diagram; determined by qRT-PCR on an extended set of mice; n = 5–7). Data are expressed as mean ± sem; *P < 0.05, **P < 0.01 by the Student’s t-test. EC, endothelial cell; HEPs, hepatocytes; HSC, hepatic stellate cell; KCs, Kupffer cells; LSEC, liver sinusoidal endothelial cell; WT, wild-type.