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. 2018 Jul 6;6:20. doi: 10.1038/s41413-018-0020-0

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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 — PKCK2 confers articular chondrocytes the ability to resist lipotoxicity through maintaining LD accumulation. a Immunohistochemistry staining of the cartilage obtained from ACLT model shows that the population of PKCK2-positive articular chondrocytes 6 weeks after surgery was significantly smaller in mice fed an HFD than in mice fed an SD. The PKCK2-positive cells were quantified (n = 4). **P < 0.01 vs. mice fed an SD according to Scheffe’s test. Scale bar, 20 μm. b Viability assay showing that FFAs sensitised chondrocytes to 100 μmol·L^-1 DRB-induced death (n = 4). *P < 0.05 and **P < 0.01 according to Scheffe’s test. c Representative western blots showing that FFAs at toxic concentrations reduced the expression level of PKCK2 protein (n = 4). d Representative western blots showing that 1 mmol·L^-1 oleate with 100 μmol·L^-1 DRB activated caspase-3 and -7 and decreased the levels of FSP27 protein (n = 4). e Representative confocal microscopy images showing that co-treatment with DRB reversed oleate-induced LD enlargement. The quantification shows that the total LD volume was significantly decreased by co-treatment with DRB (n = 4). **P < 0.01 vs. 1 mmol·L^-1 oleate treatment according to Scheffe’s test. Scale bar, 10 μm. f Viability assay showing that cilostazol (Cilo) pre-treatment prevented 1.5 mmol·L^-1 oleate-induced cell death (n = 4). **P < 0.01 vs. oleate alone treatment according to Scheffe’s test. g Representative histograms showing that 30 μmol·L^-1 cilostazol prevented 1.5 mmol·L^-1 oleate-induced apoptosis (n = 4). h Representative western blots showing that 30 μmol·L^-1 cilostazol prevented the 1.5 mmol·L^-1 oleate-induced downregulation of FSP27 and activation of caspase-3 and -7 (n = 4). i Representative confocal microscopy images showing that cilostazol prevented oleate-induced LD fragmentation (n = 4). The quantification shows that the total LD volume was significantly increased by cilostazol. **P < 0.01 vs. 1.5 mmol·L^-1 oleate alone treatment according to Scheffe’s test. Scale bar, 10 μm