Figure 7: Impact of SMIT1 deletion on HG-induced NOX2 activation and ROS production. | Scientific Reports

Figure 7: Impact of SMIT1 deletion on HG-induced NOX2 activation and ROS production.

From: Sodium-myoinositol cotransporter-1, SMIT1, mediates the production of reactive oxygen species induced by hyperglycemia in the heart

Figure 7

(A) LVEDV, (B) EF and (C) LV mass were measured by echocardiography of SMIT1 WT (n = 10) and KO (n = 10) mice. Echocardiographic data in M-mode and 2D parasternal long axis are presented in Supplementary Table 5. (D) Detection of SGLT1, SGLT2, SGLT3b, SGLT4, SGLT5 and SGLT6 by RT-PCR and ethidium bromide-stained agarose gels on mRNA extracted from the hearts of SMIT1 KO mice (n = 3) compared to WT mice (n = 3). Positive controls were intestine for SGLT1, kidneys for SGLT2, SGLT3, SGLT4 and SGLT5, brain for SGLT6 and SMIT1. (E) Quantification of HG-induced p47phox translocation close to cav3 in SMIT1 WT mice compared to SMIT1 KO mice. Adult mouse cardiomyocytes were isolated from SMIT1 WT (n = 4) or SMIT1 KO (n = 4) hearts. PLA was performed 90 min after stimulation with HG and compared to 5 mM of glucose. White lines correspond to 20 μm. (F) ROS production induced by 3 h of incubation with HG in cardiomyocytes isolated from SMIT1 WT (n = 6) or SMIT1 KO (n = 6) mice. (G) Cardiac glucose uptake in SMIT1 WT (n = 6) vs KO (n = 6) mice was measured under LG, HG and after insulin (3.10−9 M insulin 30 min). Data are means ± SEM. Statistical analysis was by two-way ANOVA (E–F). $Indicates values statistically different from LG, p ≤ 0.05.

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