Fig. 5
STAMP2 confers articular chondrocytes the ability to resist lipotoxicity through maintaining LD accumulation. a Representative western blots showing that STAMP2 was substantially expressed in rat articular chondrocytes (Chon) (n = 4). Liver, adipose (Adip) and heart tissue were used as positive controls. b Immunohistochemistry staining of the cartilage obtained from ACLT model shows that the population of STAMP2-positive articular chondrocytes 6 weeks after surgery was significantly smaller in mice fed an HFD than in mice fed an SD. The STAMP2-positive cells were quantified (n = 4). **P < 0.01 vs. mice fed an SD according to Scheffe’s test. Scale bar, 20 μm. c Representative western blots showing that oleate, palmitate or stearate at toxic concentrations reduced the expression level of STAMP2 (n = 4). d Viability assay showing that STAMP2-depletion significantly sensitised chondrocytes to lipotoxicity (n = 4). **P < 0.01 vs. scRNA according to Scheffe’s test. e The knockdown of STAMP2 reduced the total LD volume. The quantification shows that the knockdown of STAMP2 significantly decreased the total LD volume. **P < 0.01 vs. scRNA control according to Scheffe’s test. Scale bar, 10 μm. f Representative western blots showing that 25 ng·mL-1 TNF-α reversed 1.5 mmol·L-1 oleate-induced downregulation of STAMP2 protein (n = 4). g Viability assay showing that 25 ng·mL-1 TNF-α prevented 1.5 mmol·L-1 oleate-induced cell death (n = 4), which was not observed in STAMP2 (ST2)-depleted cells. **P < 0.01 vs. 1.5 mmol·L-1 oleate alone treatment. h TNF-α reversed 1.5 mmol·L-1 oleate-induced reduction of LD size and total LD volume. **P < 0.01 vs. 1.5 mmol·L-1 oleate alone treatment. Scale bar, 10 μm
