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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. 4 — a HSP60 restored the glucocorticoid-mediated loss of phosphorylated ERK, phosphorylated Ser473-Akt, and phosphorylated RPTOR abundances. b It attenuated glucocorticoid-enhanced Bax, cytochrome c, and cleaved caspase3 levels. c Forced HSP60 expression alleviated the glucocorticoid elevation of protein aggregation along with decreased RPTOR aggregation. Actin immunoblots indicate equal amount of cell lysates pipetted for protein aggregation assay. d, e HSP60 overexpression reduced the glucocorticoid-upregulated levels of ubiquitinated proteins and RPTOR. Knocking down HSP60 impaired RPTOR phosphorylation but increased RPTOR aggregation and ubiquitination. f MG132 attenuated the glucocorticoid-induced RPTOR ubiquitination and restored RPTOR and LC3-II levels and LC3-II/LC3-I ratio. g Images of TUNEL staining in osteoblasts. HSP60 and RPTOR attenuated glucocorticoid-mediated apoptosis. Scale bar, 85 μm. Experiments results are expressed as mean ± standard error. Asterisks (*) resemble a significant difference (P < 0.05) vs. scramble group, and hashtag (#) indicates a distinguishable difference (P < 0.05) vs. glucocorticoid-treated group