Striatin heterozygous mice are more sensitive to aldosterone-induced injury

Figures

• 

  Figure 1. Blood pressure and activation of RAAS after 3 weeks of treatment. (A) Delta systolic BP measured as treatment BP minus baseline BP, n = 7–8/group. Data represent mean ± s.e.m. (B) Plasma renin activity (PRA) and (C) plasma aldosterone were measured by radioimmunoassay. Statistical analysis performed using one-way ANOVA with a post hoc Bonferroni’s multiple comparison test, * = P < 0.05, ** = P < 0.01,*** = P < 0.001 compared to vehicle and n = 5–8/treatment group.

• 

  Figure 2. MR genomic markers of renal sodium signaling. (A) MR, (B), αENaC, (C) SGK1, (D) Nedd4l and (E) Rac1 as measured by Nanostring Technologies. n = 5–6. Data presented at mean ± s.e.m. ns = P > 0.05, * = P < 0.05, ** = P < 0.01, ***P < 0.001.

• 

  Figure 3. Renal injury. (A) Urine albumin/creatinine ratio was measured using DCA systems microalbumin/creatinine regent kit. (B) Estimated glomerular volume was performed by Periodic acid-Schiff (PAS). (C) Representative glomeruli section, magnification 600×. Data presented as mean ± s.e.m., n = 6–8 mice/group. (D) pAkt/Akt renal cortex protein analysis by western immunoblot. Data presented as mean ± s.e.m., n = 6–8 mice/group. Statistical analysis, * = P < 0.05, ** = P < 0.01, *** = P < 0.001 one-way ANOVA analysis comparing treatment groups within each genotype.

• 

  Figure 4. Aldosterone-induced biomarkers of damage. (A) Collagen type I alpha 1 (Col1a1), (B) C-C motif chemokine ligand 2 (CCL2). As measured by Nanostring Technologies. n = 5–6. Data presented at mean ± s.e.m. ns = P > 0.05, * = P < 0.05, ** = P < 0.01, ***P < 0.001.

• 

  Figure 5. Cardiac tissue analysis myocardial damage, H&E staining, magnification at 200×.

• 

  Figure 6. The effect of L-NAME/AngII treatment on blood pressure and RAAS. (A) Delta SBP was measured as a change from day 11 minus day baseline. (B) Plasma aldosterone and (C) plasma renin activity (PRA) were measured by radioimmunoassay. Statistical analysis performed using one-way ANOVA with a post hoc Bonferroni’s multiple comparison test, * = P < 0.05, ** = P < 0.01, *** = P < 0.001 compared to vehicle and n = 5–8/treatment group. One-way ANOVA with Bonferroni post hoc analysis compared to the control group within each genotype *P < 0.05, **P < 0.01, ***P < 0.001; n = 6–13.

• 

  Figure 7. Cardiac injury assessment following L-NAME/AngII treatment. (A) Heart weight (HW) to body weight (BW) ratio was measured after 11 days of treatment. (B) Cardiac damage score using a scale from 1 to 4. (C) Representative myocardial macrophage infiltration and necrotic lesions, hematoxylin and eosin; magnification, ×20. One-way ANOVA, Bonferroni multiple comparison post-hoc to control group within each genotype, *P < 0.05, **P < 0.01 and ***P < 0.001; n = 4–10.

• 

  Figure 8. The effect of L-NAME/Ang II on renal injury. (A) Whole kidney weight to body ratio after 11 days of treatment. (B) Urine albumin/creatinine ratio was measured using DCA systems microalbumin/creatinine regent kit. (C) Periodic acid-Schiff (PAS) stained tissues were used to assess glomerular volume. (D) Representative glomeruli section H&E Staining, magnification 600×. Data presented as mean ± s.e.m., n = 6–8 mice/group. Data presented as mean ± s.e.m., n = 6–8 mice/group. Statistical analysis, * = P < 0.05, ** = P < 0.01 one-way ANOVA analysis comparing treatment groups within each genotype.