Extended Data Fig. 7: 11,12-EET propels MuSC proliferation via enhancing FGF-FGFR signaling.
From: Gasdermin D-mediated metabolic crosstalk promotes tissue repair
a, Correlation between gene fold-changes of 11,12-EET versus control, and gene fold-changes of activated versus quiescent MuSCs (from GSE113631). b, Dotplot of expressions of growth factor receptor genes in different MuSC celltype from scRNAseq data of Fig. 2b. c,d Immunoblots of the PI3K-AKT-mTOR and MAPK signaling pathways downstream of FGF-FGFR in NIH-3T3 cells treated with bFGF with/without 11,12-EET (c), or with vehicle, 11,12-EET or 11,12-EET + FGFR inhibitor (d). e, Immunoblots of EGFR activation in NIH-3T3 with or without 11,12-EET. f,g, Analysis pipeline of the correlation level between each gene and FGF signaling score (f) and GO enrichment with the top 300 correlated genes (g), related to Fig. 5d. FGF signaling score was determined using AddModuleScore with gene set ‘RESPONSE_TO_FIBROBLAST_GROWTH_FACTOR’. h, Representative images of FGF condensates on cell surface. Scale bars, 10 μm. i, Immunoblots of eGFP-bFGF oligomerization in NIH-3T3 cells after FGF treatment with/without 11,12-EET.j, Schematic of 11,12-EET treatment and scRNAseq design. k,l, Immunoblots of the PI3K-AKT-mTOR and MAPK signaling pathways downstream of FGF-FGFR in TA muscles subjected to CTX-induced injury with vehicle, vehicle+FGFR inhibitor, 11,12-EET or 11,12-EET + FGFR inhibitor intramuscularly treatment (k), or from Ephx2f/f and Ephx2CKO mice at 3 dpi (l). A representative (c-e,h,i,k,l) of at least two independent experiments is shown. Pearson correlation analysis for (a). Abbreviation: FGFRi, FGFR inhibitor.
