Fig. 5
SPI1 activates the UPRmt via PERK and inhibits chondrocyte senescence rather than by activating GCN2. a Protein expression of SPI1, PERK, p16INK4A, p21, GLB1, GCN2, eIF2α, p-eIF2α, ATF5, HSP60, LONP1 and ClpP was detected by WB in chondrocytes with SPI1 overexpression in model groups. The ratio of p-eIF2α to eIF2α is shown. b Gene expression changes of SPI1, PERK, CDKN2A, CDKN1A, GLB1, GCN2, eIF2α, ATF5, HSP60, LONP1 and ClpP was detected by RT-qPCR in chondrocytes with SPI1 overexpression in model groups. c Protein expression of SPI1, PERK, p16INK4A, p21, GLB1, GCN2, eIF2α, p-eIF2α and ATF5 were detected by WB in chondrocytes with SPI1 inhibition in model groups. The ratio of p-eIF2α to eIF2α is shown. d Gene expression changes of SPI1, PERK, CDKN2A, CDKN1A, GLB1, GCN2, eIF2α and ATF5 were detected by RT-qPCR in chondrocytes with SPI1 inhibition in model groups. The cell sample size is n = 4. Experiments were independently repeated three times. The data were expressed as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 versus the Control group, ns indicates not significant. t-test
