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. 2023 Feb 22;6:208. doi: 10.1038/s42003-023-04563-1

Fig. 5. Circulating Klotho mediates its effects through the regulation of ER stress/UPR pathways in response to NTS-induced injury.

Fig. 5

a Venn diagrams illustrate the number of genes significantly regulated by Klotho overexpression in glomeruli-enriched or tubuli-enriched (ROK) fractions as well as their overlap in Alb-hKL compared to WT animals. b Functional enrichment analyses (GO-term analysis on the left panel; KEGG pathway analysis on the right panel) conducted on the upregulated genes in the glomerular fraction shown in (a). Only significant enrichments are shown (DAVID scores ≥1.3). Black boxes highlight the GO-term and KEGG pathways which we focused on in further analyses. c, d Representative western blotting (left panels) of GRP78/BiP (c) and LC3B (d) in glomeruli-enriched lysates from the different groups. 20 μg of proteins per well were loaded. Densitometry quantification (right panels) for GRP78/BiP and LC3B (n = 5 WT-control; n = 6 WT-NTS; n = 5 Alb-hKL-NTS) was performed. #p < 0.05, ##p < 0.01 vs. WT-control; @p < 0.05 vs. WT-NTS. e, f Representative western blotting (left panels) of GRP78/BiP (e) and LC3B (f) in immortalized mouse podocytes after treatment with tunicamycin (5 μg/ml) and/or recombinant human Klotho (r-hKlotho, 0.05 μg/ml) for 16 h. 10 μg of proteins per well were loaded. Densitometry quantification (right panels) was performed on 3 replicates for each condition. *p < 0.05; **p < 0.01; ***p < 0.001. Statistical significance between groups was determined using one-way ANOVA.