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. 2019 Nov 16;31:138–149. doi: 10.1016/j.molmet.2019.10.008

Figure 4.

Figure 4

FPR2 deletion developed age-related cardiorenal syndrome with signs of unresolved and chronic inflammation. (A, B, C) mRNA expression profiling of proinflammatory cytokines (Ccl2, IL1-β, and TNF-α) in the LV of FPR2−/− and WT mice. (D) Periodic acid–Schiff (PAS) staining showing structural changes in the kidney at 7 months of age in WT and FPR2−/− mice (magnification = 40×; scale = 50 μm). (E) Increased plasma creatinine levels in FPR2−/− mice compared with WT at 7 months of age. (F) Kidney mRNA expression of injury marker NGAL in WT and FPR2−/− mice at 2 and 7 months of age. (G) Picrosirius red (PSR)–stained kidney showing fibrotic remodeling and collagen deposition in FPR2−/− mice at 2 and 7 months compared with age-matched WT controls (magnification = 40×; scale = 50 μm). (H) High collagen content in the cortex area of the kidney in FPR2−/− mice compared with WT mice at 2 and 7 months of age. (I, J, K) Immunofluorescence images presenting altered kidney structure stained using WGA (green), increased NGAL (red), and vimentin (red) staining in FPR2−/− mice compared with WT controls at 7 months of age. Nuclei are stained blue with Hoechst (magnification = 40×; scale = 50 μm). (L, M, N) mRNA expression of proinflammatory genes (Ccl2, IL1-β, and TNF-α) in the kidney of FPR2−/− and WT mice at 2 and 7 months of age. *p < 0.05 vs WT. Values are means ± SEM; n = 5–9 mice/group.