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. 2017 Mar 27;28(8):2443–2458. doi: 10.1681/ASN.2016070711

Figure 4.

Figure 4.

Evidence from isolated glomeruli suggests that ETA receptor antagonism prevents the onset of glomerular inflammation and oxidative stress in humanized sickle cell mice. Expression of components of the ET system, inflammation, and oxidative stress in glomeruli from genetic control (HbAA) and humanized sickle mice (HbSS) treated with vehicle, the selective ETA antagonist, ambrisentan, or the combined ETA/B antagonist, A-182086, for 10 weeks beginning at 4 weeks of age. (A) Depicts the relative ET-1 mRNA expression in glomeruli after 10-week treatment protocol. (B) Depicts the relative ETA receptor mRNA expression in glomeruli after 10-week treatment protocol. (C) Depicts the relative ETB receptor mRNA expression in glomeruli after 10-week treatment protocol. (D) Depicts the relative P-selectin mRNA expression in glomeruli after 10-week treatment protocol. (E) Depicts the relative vascular cell adhesion molecule 1 (VCAM-1) mRNA expression in glomeruli after 10-week treatment protocol. (F) Depicts the relative monocyte chemoattractant protein-1 (MCP-1) mRNA expression in glomeruli after 10-week treatment protocol. (G) Depicts the glomerular ROS production after 10-week treatment protocol. Data are mean±SEM; *P<0.05 versus vehicle-treated HbAA; #P<0.05 versus vehicle-treated HbSS; n=5–6 in HbSS and n=6 in vehicle-treated HbAA group. AUC, area under the curve.