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. 2021 Jul 22;12:4452. doi: 10.1038/s41467-021-24736-y

Fig. 1. S-nitrosylation of GNAI2 is significantly higher in diabetes-accelerated atherosclerosis in vitro and in vivo.

Fig. 1

a A biotin-switch assay detected protein S-nitrosylation in HUVECs treated with Mannitol+nLDL or HG (25 mmol/L) and oxLDL (50 μg/mL). One independent experiment was performed. b S-nitrosylation of GNAI2 is significantly higher in coronary arteries of diabetic patients with CAD. The level of SNO-GNAI2 was quantified with total-GNAI2 and normalized to Control patients. n = 5 distinct samples for each group. c S-nitrosylation of GNAI2 is increased in the aortas of LDLr−/− mice treated with STZ and HFD. The level of SNO-GNAI2 was quantified with total-GNAI2 and normalized to Vehicle + NC mice. n = 6 distinct samples for each group. d S-nitrosylation of GNAI2 is markedly increased in HUVECs treated with HG and oxLDL for 24 h. The level of SNO-GNAI2 was quantified with total-GNAI2 and normalized to Mannitol+nLDL-treated cells. n = 3 distinct samples for each group. N.D represents no detected. e S-nitrosylation of GNAI2 is significantly increased in HAECs treated with HG and oxLDL for 24 h. The level of SNO-GNAI2 was quantified with total-GNAI2 and normalized to Mannitol+nLDL-treated HAECs. n = 3 distinct samples for each group. N.D represents no detected. Data are represented as the Mean ± SEM. Unpaired two-tailed Student’s t-test was used for statistical analysis. Source data are provided as a Source Data file.