Skip to main content
. Author manuscript; available in PMC: 2022 Oct 6.
Published in final edited form as: Sci Transl Med. 2022 Apr 6;14(639):eabe5795. doi: 10.1126/scitranslmed.abe5795

Figure 4. P2Y14 promotes HSC activation via ERK and YAP.

Figure 4.

A. RNA-seq and gene set enrichment pathway analysis and a heatmap of the top 6 genes in primary BALB/c mouse HSCs treated with UDP-glucose (10 μM) for 24h (n=3 technical replicates /group). B-C. qPCR for YAP target genes after 24h (B) or immunofluorescence for YAP after 2h (C) of UDP-glucose (10 μM) treatment (n=1-3 technical replicates /condition). D. qPCR for Acta2 in YAPfl/fl or YAPΔHSC HSC, treated with 10 μM UDP-glucose (n=2-4 technical replicates /condition). E. Yap deletion in mouse HSCs from 6-times CCl4-treated mice (n=1 per condition). F. Phospho-pathway screen in mouse HSCs treated with 10 μM UDP-glucose for 15 minutes. G-I. Western blot for phospho- and total ERK in (G) mouse HSCs treated with various concentrations of UDP-glucose, UDP-galactose or UDP-glucuronic acid for 15 minutes, (H) mouse HSCs treated with 10 μM UDP-glucose for various times (n=1 per concentration or time point), or (I) primary mouse HSCs, hepatocytes, macrophages and LSECs treated with 100 μM UDP-glucose. J-K. Effect of MEK inhibitor PD98059 on UDP-glucose-induced αSMA expression after 48h (J) or Acta2 mRNA after 24h treatment (K) (n=3 technical replicates/condition). Data are shown as means ± SEM. Scale bar 20 μm.