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. 2019 Nov 5;7:34. doi: 10.1038/s41413-019-0070-y

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 9 — Osteocyte deficiency of MMP13 causes dysregulation of genes related to matrix degradation and acidification. a RNA-seq of wild-type and MMP13^ocy−/− mice (n = 4) identified differentially expressed genes (DEGs) that are significantly repressed (blue) or induced (red) in MMP13^ocy−/− bone, with downregulation of MMP13 and upregulation of several proteases and acidification-related genes (highlighted in turquoise). Transcription factors and other genes implicated in osteoblast differentiation (yellow) are among the genes that did not show significant expression differences in MMP13^ocy−/− bone (gray). b Genes related to acidification were hierarchically clustered in a heatmap by z-score. c qPCR of wild-type (n = 8) and MMP13^ocy−/− (n = 6) bone validates both co-regulated and compensatory expression of PLR genes (mean ± SD). d Immunohistochemistry reveals increased levels of Cathepsin K in osteocytes in MMP13^ocy−/− cortical bone (scale bars 50 μm). *P < 0.05 between genotypes by unpaired t test