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. 2018 Jan 16;9(1):e02217-17. doi: 10.1128/mBio.02217-17

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Copyright © 2018 Lee et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

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FIG 6 — Alteration of the global gene expression of LECs by vIRF3 and the essential role of HDAC5 for vIRF3-mediated sprouting formation. (A) (Left panel) Principal component plot of both lymphatic endothelium gene expression and blood endothelium gene expression profiles upon vIRF3 expression. Numbers in brackets indicate percentages of total variation explained by each principal component (PC). (Right panel) Venn diagram showing the number of significantly up- and downregulated genes upon vIRF3 expression in LECs and BECs. (B and C) Gene set enrichment analysis (GSEA) of genes significantly up- or downregulated upon vIRF3 induction in LECs (B) and BECs (C), respectively. Positive normalized enrichment scores (NES) indicate increased pathway activity, and negative scores indicate decreased pathway activity. (D and E) The essential role of HDAC5 in vIRF3-induced sprouting formation. Phase-contrast images are shown. (D) LEC-E6/E7 V5/vIRF3 cells were transfected with siRNA as a control (Scramble) or with HDAC5-specific siRNA for 48 h, followed by embedding into matrigel. NC, negative control. (E) Sprouting of LEC-E6/E7 V5/vIRF3 spheroids treated with 5 μM MC1586 (HDAC5 inhibitor).