Fig. 6: Zfp36 overexpression in senescent mouse macrophages accelerated IL-27 p28 mRNA degradation and reduced IL-27 release. | Cell Discovery

Fig. 6: Zfp36 overexpression in senescent mouse macrophages accelerated IL-27 p28 mRNA degradation and reduced IL-27 release.

From: Senescence-induced p21high macrophages contributed to CD8+ T cells-related immune hyporesponsiveness in kidney transplantation via Zfp36/IL-27 axis

Fig. 6

a Venn diagram showing the overlap of Zfp36 target genes in p21high macrophages, upregulated genes in the Young WT group compared to Old WT, and upregulated genes in the Young WT group compared to Old G3 Terc−/−. b Expression level of IL-27 p28 in macrophages of Young WT, Old WT, and Old G3 Terc−/− mouse allografts. c IL-27, IL-10, IL-12 and IL-23 levels in mouse serum 7 days after surgery by ELISA, n = 3/group. d Expression level of BMDM IL-27 p28 at rest or stimulated by LPS analyzed using qPCR, n = 5/group. e IL-27 p28 and ACTB mRNA degradation analyzed using qPCR after blocking RNA de novo synthesis using ActD, n = 5/group. f PAR-iCLIP coverage for IL-27. g Confocal microscopy analysis of the colocalization of Zfp36 (green) and IL-27 p28 mRNA (red). Scale bar, 50 μm. h IL-27 levels in BMDM supernatants of Young WT, Old WT, and Old G3 Terc−/− mice by ELISA, n = 5/group. i IL-27 levels in supernatants of BMDM with or without irradiation detected by ELISA, n = 5/group. j IL-27, IL12 and IL23 levels in WT and Lyz2-cre;Zfp36f/f mice, n = 3/group. Data are presented as mean ± SD. Statistical analysis was performed using two-tailed Student’s t-test (b–d, g–i) or Two-Way ANOVA (e). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, NS, not significant. BMDM, bone marrow-derived macrophages.

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