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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: J Bone Miner Res. 2016 Apr 20;31(9):1652–1665. doi: 10.1002/jbmr.2848

Figure 1.

Figure 1

Injury triggers hypoxia in early FOP lesions. (A) Nuclear localization of HIF-1α by immunohistochemistry in tissues sections from unaffected individuals (n = 4) and those with FOP (n = 6). Magnified images of the indicated regions of interest are shown in the right-most panels. Scale bar, 50 µm. Dashed circles delineate centralization of nuclei in degenerating muscle. (B) Quantification of HIF-1α positive cells from normal human muscle and stage-specific early FOP lesional tissue, expressed as the percentage of cells with nuclear HIF-1α (DAPI and HIF-1α co-localization). (C) Identification of hypoxia in early FOP lesions induced by Adenovirus-Cre and cardiotoxin in a caACVR1 FOP-like mouse model (n = 3). The no 1° antibody (negative) control was performed on lesional tissue seven days after injury. Scale bar = 100 µm.