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. 2022 Mar 17;13:1439. doi: 10.1038/s41467-022-29150-6

Fig. 3. SMO agonist treatment promotes MuSC expansion.

Fig. 3

a SMO agonists SAG1.3 and purmophamine promote MuSC proliferation in a dose-dependent manner (n = 3–4 biological replicates per condition, isolated from independent mice and each performed in 3 technical replicates). b Proliferation of control or IFT88−/− MuSCs treated with vehicle (veh) or SMO agonist SAG1.3 (50 nM), shown as fold change normalized to control vehicle treated (n = 5 control veh, 4 control SAG1.3, 8 IFT88−/− veh, 6 IFT88−/− SAG1.3). c Percentage of EdU+ vehicle or 5 µM cyclopamine (SMO antagonist) treated MuSCs (n = 3 mice per condition). d Vismodegib (100 nM, SMO antagonist) inhibits MuSC proliferation as determined by Vision Blue assay (n = 7 veh and 3 vismodegib treated). e, f Expansion of endogenous MuSCs in Pax7CreERT2;Rosa26-LSL-Luc mice treated with tamoxifen (TAM) to label resting MuSCs and assayed by BLI post-notexin injury. e Experimental scheme. f Left: BLI (n = 8 mice per condition, individual data points in Supplementary Fig. 3a). Right: Representative BLI image. *P < 0.05, **P < 0.01, ***P < 0.001. Mann–Whitney test (c, d). ANOVA test with Fisher’s LSD for multiple comparisons (a, b). Significance relative to vehicle (0 nM) (a); 2 way ANOVA test with Fisher’s LSD for multiple comparisons per time point (f). Source data are provided as a Source Data file. Means+s.e.m.