Fig. 3: AB-EVs promote bone-fat imbalance in young and aged mice.
From: Aged bone matrix-derived extracellular vesicles as a messenger for calcification paradox
a Schematic diagram of the experimental design for assessing the effects of YB-EVs and AB-EVs on bone phenotypes in young and aged mice. b μCT-reconstructed images of femurs. Scale bars: 1 mm. c Quantification of Tb. BV/TV, Tb. N, Tb. Th, and Tb. Sp. n = 10 biologically independent animals per group. d Ultimate load values of femurs. n = 10 biologically independent animals for young mice. n = 6 biologically independent animals for aged mice. e–f, Calcein (green) double labeling of trabecular bones (e) and quantification of BFR/BS and MAR (f). Scale bar: 25 μm. n = 5 biologically independent animals per group. g–h, PLIN immunofluorescence staining images of femur sections (g) and quantification of the number of PLIN+ (red) adipocytes in bone marrow (h). Scale bar: 100 μm. n = 6 biologically independent animals per group. i qRT-PCR for Pparγ expression in femurs. n = 9 biologically independent animals per group. j–k, OCN immunohistochemical staining images (j) and the number of OCN-stained (brown) osteoblasts (N. OBs) on the trabecular bone surface (BS) (k). Scale bar: 50 μm. n = 6 biologically independent animals per group. l ELISA for serum OCN. n = 10 biologically independent animals per group. All experiments were performed with at least five biological replicates per group without independent repetition. Data were presented as mean ± SD. Statistical significance was determined by one-way ANOVA with Bonferroni post hoc test. Source data are provided as a Source Data file.
