Figure 4: Dysregulation of TGF-β signalling drives the phenotype in GOF mice. | Nature Communications

Figure 4: Dysregulation of TGF-β signalling drives the phenotype in GOF mice.

From: MicroRNA miR-23a cluster promotes osteocyte differentiation by regulating TGF-β signalling in osteoblasts

Figure 4

(a) Representative luminescence images of TGF-β reporter mice (P3) harbouring different transgenes. TGF-β reporter activity in the head is from active bone formation in the postnatal growing cranium. 23aC, Col1a1-miR-23aC; 23D, Col1a1-miR-23a decoy; 27D, Col1a1-miR-27a decoy. (b) Luminescence quantification shows increased activity of TGF-β signalling in Col1a1-miR-23aC (23aC) mice and decreased activity in Col1a1-miR-23a decoy (23D) and Col1a1-miR-27a decoy (27D) mice (N=4 for each group). (c) μCT analysis of BV/TV in lumbar spines. The low bone mass phenotype in Col1a1-miR-23aC mice was rescued by anti-TGF-β antibody treatment (23aC 1D11) to levels comparable with those in WT mice treated with control antibody (WT13C4; 12-week old females; N=4 for each group). (d) Representative trichrome staining images of spines showing osteocyte (white arrows) density in Col1a1-miR-23aC (23aC) and WT littermates treated with 1D11 or 13C4. White bars indicate scale of 100 μm. (e) Osteocyte density (OT.N/Bone area) measured by bone histomorphometric analysis. Osteocyte density in Col1a1-miR-23aC mice was reduced by 1D11 (23aC 1D11) compared to 13C4 (23aC 13C4; N=4 for each group). Statistical analyses used t-test for paired groups and one-way ANOVA for multiple groups. Data are shown as mean±s.d.; *P<0.05, **P<0.01, ****P<0.001.

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