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Journal: iScience
Article Title: HSV-1 alters lipid metabolism and induces lipid droplet accumulation in functionally impaired mouse dendritic cells
doi: 10.1016/j.isci.2025.112441
Figure Lengend Snippet: Yield of infectious HSV-1 and viral protein synthesis in BMDCs treated with inhibitors of lipid-metabolism-related enzymes Plaque-forming units (PFUs) and viral protein expression analyses (western blot) of HSV-1 late viral proteins (glycoprotein B, glycoprotein D, and VP16) in BMDCs treated for 3 h with the (A) DGAT1 inhibitor A-922500 (10 μM) (B) DGAT2 inhibitor PF-06424439 (10 μM), (C) ACAT inhibitor avasimibe (10 μM), (D) ACS inhibitor TOFA (10 μM), (E) ACS inhibitor triacsin C (10 μM), (F) lipase inhibitor CAY10499 (10 μM), (G) FATP inhibitor lipofermata (10 μM), or (H) CD36 inhibitor sulfosuccinimidyl oleate (SSO, 50 μM) and then infected with HSV-1 strain F at MOI 3 for 12 hpi or 18 hpi. (−) corresponds to vehicle treatment (DMSO) and (+) to treatment with the inhibitor. C + corresponds to Vero-HSV-1-infected cells (positive control). The analyses shown are means ± SEM of three independent assays. The statistical analyses were performed using two-way ANOVA and Bonferroni multiple comparisons test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: no statistical significance). See also Figure S5 .
Article Snippet: The lipid metabolism inhibitors (all from Cayman chemical) were lipofermata-10 μM (FATP inhibitor), sulfosuccinimidyl oleate-50 μM (SSO-CD36 inhibitor), 5-(tetradecycloxy)-2-furancarboxylic acid (TOFA)-10 μM (ACC inhibitor), Triacsin C-10 μM (ACS inhibitor), A922500-10 μM (DGAT1 inhibitor), PF-06424439-10 μM (DGAT2 inhibitor), Avasimibe-10 μM (ACAT1 and ACAT2 inhibitor) and CAY10499-10 μM (Lipase inhibitor).
Techniques: Expressing, Western Blot, Infection, Positive Control