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. 2017 Oct 23;8:1346. doi: 10.3389/fimmu.2017.01346

Figure 9.

Figure 9

Induction of Prss35 by IL-36α stimulation in vitro and unilateral ureter obstruction (UUO) kidneys in vivo. (A) Genes downregulated (twofold down) in microarray in the kidneys of IL-36α- knockout (KO) mice compared with that in WT mice at 48 h after UUO. (B) Relative mRNA expression of genes downregulated in panel (A) in IL-36α-exposed NIH3T3 cells. Values = mean ± SE (n = 4). A significant difference with 0 h is indicated by *(P < 0.05). (C) mRNA expression of Prss35 in IL-36α-exposed NIH3T3 cells. (D) Relative mRNA expression of Prss35 in IL-36α-exposed NIH3T3 cells. Values = mean ± SE (n = 4). A significant difference with 0 h is indicated by *(P < 0.05). (E) Immunoblotting for Prss35 and β-actin using cell lysates from NIH3T3 cells after IL-36α exposure for 0 and 48 h. (F) Prss35 levels in cell lysate from IL-36α-exposed NIH3T3 cells. Values = mean ± SE (n = 4). A significant difference with 0 h is indicated by *(P < 0.05). (G) Immunohistochemistry for Prss35 in Cont and UUO kidneys of WT mice. Prss35+ staining was strong in interstitial fibroblasts in the kidneys of UUO at 4 days after operation. No positive reaction is observed in IgG-isotype control staining.