Fig. 1 | Signal Transduction and Targeted Therapy

Fig. 1

From: Targeting cellular senescence prevents glucocorticoid-induced bone loss through modulation of the DPP4-GLP-1 axis

Fig. 1

Eight-week-old C57 male mice were injected with Pred (2.5 mg/kg/d) or vehicle (ac). Femur sections of the indicated groups were subjected to immunofluorescence staining and SA-βGal staining. Representative images of SA-βGal+ cells (blue) in metaphysis are shown in a. Femur sections of the indicated groups were subjected to immunofluorescence staining with Ki67 (red) antibodies (b). The sections of femurs were stained with anti-p16 antibodies (red) (c). Dasatinib and quercetin (D + Q) treatment (df). Representative micro-CT images of distal femurs (d, longitudinal sections). Representative SA-βGal+ cell staining (blue) images are shown in e. The number of SA-βGal+ cells per trabecular bone surface (N. SA-βGal+ cells/ Ar) is quantified in f. Immunofluorescence staining. Colocalization of LepR (green) with p16INK4a (red) (g). Analysis of DPP4 activity (h) and GLP-1 levels in plasma (i). mRNA levels of GLP-1R in LepR+ MSCs (j). GC induced LepR+ cell senescence through the DPP4/GLP-1 axis, modulating the AMPK-SIRT1-FOXO3a pathway. Inhibition of senescent cells or the proinflammatory secretome restores bone homeostasis in GIOP mice. GCs Glucocorticoids, TNFα KO TNFα Knockout mice, IL6 KO IL-6 Knockout mice, D + Q Dasatinib and quercetin, JAKi Ruxolitinib, GIOP glucocorticoid-induced osteoporosis (k). GP growth plate, Ar tissue area. DAPI was used to stain nuclei blue. *p < 0.05, **p < 0.01

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