In sickle cell mice, 17R-RvD1 reduces proangiogenic signaling, prevents H/R-induced ER stress, and protects against proapoptotic H/R-induced signature. (A) Serum Gal-3 (left) and procollagen C-proteinase enhancer-1 (PCPE1) in SS mice treated with either vehicle or 17R-RvD1 at 3 days after H/R stress. Data are presented as mean ± SEM (n = 3-4). ∗P < .05; ∗∗∗P < .005 (by unpaired t test, with Welch correction). a-SMA (B) and Picrosirius Red (C) staining in cardiac slices from SS mice treated with either vehicle or 17R-RvD1 at 3 days after H/R stress. (D) Immunoblot analysis using specific antibodies against ATF6, GADD34, ATF4, and CHOP in the hearts of AA and SS mice under normoxia, treated with vehicle or 17R-RvD1 (100 ng), and exposed to H/R: hypoxia (8% oxygen; 10 hours), followed by reoxygenation (21% oxygen; 3 hours). One representative gel from 4 gels with similar results is shown; 75 μg/μL of protein loaded on an 11% T, 2.5% C polyacrylamide gel. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) serves as protein loading control. Densitometric analysis of immunoblots is shown (right). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); °P < .05 (compared with vehicle-treated mice by 1-way ANOVA). (E) Immunoblot analysis using specific antibodies against caspase-3 in the hearts of AA and SS mice under normoxia, treated with vehicle or 17R-RvD1 (100 ng), and exposed to H/R: hypoxia (8% oxygen; 10 hours), followed by reoxygenation (21% oxygen; 3 hours). One representative gel from 4 gels with similar results is shown; 75 μg/μL of protein loaded on an 11% T, 2.5% C polyacrylamide gel. GAPDH serves as protein loading control. Densitometric analysis of immunoblots is shown (lower). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia). °P < .05 (compared with vehicle-treated mice by 1-way ANOVA). Wb, Western blot.