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. 2018 Sep 17;9(10):938. doi: 10.1038/s41419-018-0970-6

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© The Author(s) 2018

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. 1 — a Glucocorticoid reduced mRNA expression, protein levels, and immunofluorescence of HSP60 in osteoblasts. Scale bar, 8 μm. b Forced HSP60 expression attenuated the glucocorticoid-induced loss of (c) osteocalcin expression and d mineralized matrix accumulation. Scale bar, 40 μm. Increasing HSP60 attenuated the glucocorticoid-mediated loss of (e) Atg4, and Atg12 expressions, (f) LC3-II levels, LC3-II/LC3-I ratio, and g autophagic puncta formation. Scale bars, 6 μm (upper panels) and 12 μm (lower panels). Knocking down HSP60 decreased autophagic marker expressions, autophagic vesicle formation, and mineralized matrix production of osteoblasts. Experiments results are expressed as mean ± standard error. Asterisks (*) resemble a significant difference (P < 0.05) vs. vehicle or scramble group, and hashtag (#) indicates a distinguishable difference (P < 0.05) vs. glucocorticoid-treated group. Veh, vehicle; GC, glucocorticoid