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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: TLR7 activation by miR-21 promotes renal fibrosis by activating the pro-inflammatory signaling pathway in tubule epithelial cells

Fig. 4

Activation of the TLR7 signaling pathway increases NF-κB activity and chemokine expression in renal tubule epithelial cells. A Gene levels of Tlr7 were measured in NRK52E cells treated with lipopolysaccharide (LPS). *p < 0.05 versus non-treated cells. B Protein levels of TLR7 were measured in NRK52E cells treated with LPS. β-actin was used as a loading control. C Protein expression of TLR7 in NRK52E cells under the LPS-treated condition was detected via immunofluorescence. D NF-κB activity in NRK52E cells treated with R837 was measured using the NF-κB promoter luciferase assay. #p < 0.05 versus pcDNA group. *p < 0.05 versus control group. E Protein levels of phosphorylated-p65 were measured in NRK52E cells treated with LPS or R837. β-actin was used as a loading control. F NF-κB activity in NRK52E cells treated with LPS and R837 was measured using the NF-κB promoter luciferase assay. #p < 0.05 versus control group. *p < 0.05 versus LPS treated group. G Relative mRNA levels of pro-inflammatory chemokines (Il6, Il8, Cxcl1, Ccl5 and Ccl3) in NRK52E cells treated with LPS or R837. #p < 0.05 versus control group. *p < 0.05 versus LPS treated group. H NF-κB activity in NRK52E cells treated with R837 and M5049 was measured using the NF-κB promoter luciferase assay. #p < 0.05 versus control group. *p < 0.05 versus R837-treated group. I Relative mRNA levels of pro-inflammatory chemokines (Il8, Cxcl1, Ccl2, and Ccl7) in NRK52E cells treated with R837 and M5049. #p < 0.05 versus control group. *p < 0.05 versus LPS treated group

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