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. 2017 Nov 2;2(21):e96034. doi: 10.1172/jci.insight.96034

Figure 9. Deletion of the Osmr gene reduces NHO following SCI in mice.

Figure 9

(A) μCT analysis of neurogenic heterotopic ossification (NHO) development 7–14 days following spinal cord injury (SCI) and intramuscular cardiotoxin (CDTX) injection in oncostatin M receptor null (Osmr–/–) mice compared with wild-type C57BL/6 control mice. Each dot represents an individual mouse, and the box-and-whisker plot shows median, 25th and 75 percentile, and minimum and maximum values. Statistical significance was confirmed using a Mann-Whitney test (P = 0.0038, 16 mice/group, experiment repeated twice). (B) Representative 3D reconstructed images of NHO in C57BL/6 and Osmr–/– mice 7 days after surgery. (C) Recombinant mouse oncostatin M (OSM) enhances in vitro osteogenic differentiation. Muscle interstitial cells, satellite cells, and bone marrow mesenchymal stromal cells (BM-MSCs) sorted from naive C57BL/6 mice were cultured for 10 days in control medium, osteogenic medium, or osteogenic medium plus mouse OSM (25 ng/ml). Quantification of Alizarin Red S staining via absorbance at 562 nm confirmed enhanced calcium deposition in interstitial cells (***P < 0.01), satellite cells (*P < 0.05), and BM-MSCs (****P < 0.001) in the presence of osteogenic media alone and significantly enhanced calcium deposition in both interstitial cells and satellite cells in the presence of osteogenic media plus OSM (****P < 0.001). Results are the mean and SDs of 2 separate experiments (n = 3 control media and n = 3–6 osteogenic media ± OSM/each experiment).