Fig. 6

AnxA2 drives FAP adipogenesis and injury-triggered lipid formation in dysferlinopathic muscle. a Oil Red O staining and b quantification of spontaneous adipogenesis of 20,000 FAPs each, isolated from 12Mo WT, B6A/J and A2-B6A/J after 10 days in culture, n = 3 replicates/genotype. Scale bar = 50 µm. c Oil Red O staining and d quantification (normalized to 20,000 FAPs) of spontaneous adipogenesis from a 1:1 mixed culture of 24Mo B6A/J FAPs (10,000 cells) with niche cells (10,000 cells) from either 24Mo B6A/J or A2-B6A/J. Scale bar = 50 µm. e Oil Red O staining and f quantification of spontaneous adipogenesis of 20,000 24Mo B6A/J FAPs left untreated or treated with 100 nM recombinant AnxA2. Scale bar = 50 µm. g Perilipin-1 staining from 10Mo A2-B6A/J TA muscles 28d after single notexin injury with (NTX + AnxA2) or without (NTX) co-administration of 10 µg recombinant AnxA2. Scale bar = 100 µm. h Quantification of total perilipin-1 area after injury. i PDGFRα staining from 10Mo A2-B6A/J TA muscles 28d after single notexin injury and administration of 10 µg recombinant AnxA2 compared to notexin injury alone. Scale bar = 20 µm. j Quantification of total PDGFRα area after injury. All data presented as mean ± SD, average Oil Red area compared across genotypes by ANOVA with Holm–Sidak multiple comparisons test, all other data compared via two-tailed t-test, *p ≤ 0.05 ***p < 0.001