Fig 2: GPR35 inhibition suppresses calpain 1/2 overexpression-induced mitochondrial dysfunction in NMVMs. A, Mitochondrial ATP production was checked by an assay kit. The result was expressed as a percentage of control (*P < 0.05, vs. others, #P < 0.05, vs. calpain 1/2 overexpression group; n = 6). B, MMP was assessed using JC-1 kit. Fluorescence intensity values were each expressed as ratios of emission at 590 to that at 530 nm. The result was expressed as a percentage of control (*P < 0.05, vs. others, #P < 0.05, vs. calpain 1/2 overexpression group; n = 6). C, The extent of ROS production in NMVMs was determined by lucigenin-enhanced luminescence assay (*P < 0.05, vs. others, #P < 0.05, vs. calpain 1/2 overexpression group; n = 6).

Fig 3: The effect of MI on the GPR35 expression in myocardium. The GPR35 mRNA (A) and protein (B) expression in myocardium following MI were detected by RT-PCR and immunoblotting (*P < 0.05, vs. sham, n = 6).

Fig 4: Expression of GPR35 is correlated with IDD. (a) RT-PCR analysis suggests that NPCs have downregulation of Collagen II and upregulation of MMP-3 when compressed with 20 kPa for 4 h. (b) RNA-seq heat map suggests an upregulation of the GPR35 gene when NPCs are compressed at the above degenerative condition. (c) IHC staining suggests a gradual increase of GPR35 expression in human NPs along with higher degeneration levels. (The data are shown as the mean ± SD. **P < 0.01 for comparisons between two groups. One-way ANOVA and Tukey's multiple comparison test were used for statistical analysis).

Fig 5: GPR35 inhibition suppresses calpain 1/2 overexpression-induced cardiac dysfunction. The cardiac function parameters including LVFS (A) and LVEF (B) were measured by echocardiography (*P < 0.05, vs. others, #P < 0.05, vs. calpain 1/2 overexpression group; n = 6).