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. 2021 Mar 1;131(5):e143645. doi: 10.1172/JCI143645

Figure 8. TGF-β1 induces TXNDC5 expression through ER stress– and ATF6-dependent transcriptional regulation.

Figure 8

(A) ER stress components including BiP and activated ATF6 (ATF6-p50) were upregulated following the treatment of TGF-β1 (10 ng/mL) in HKFs (n = 3). (B) ER stress inhibitor 4-PBA blocked TXNDC5 transcript upregulation induced by TGF-β1 (10 ng/mL) (n = 6–8). (C) Quantitative real-time PCR showed effective ATF6 knockdown by shATF6 in HKFs (n = 6). (D) Depletion of ATF6 reversed TXNDC5 transcript upregulation induced by TGF-β1 (10 ng/mL) (n = 6). (E) In NIH-3T3 cells, TGF-β1 treatment increased the transcriptional activity of WT but not ATF6 binding–deleted mouse Txndc5 promotor (n = 24). Data are representative of 3 or more independent experimental replicates. For all panels, data are presented as mean ± SEM. The statistical significance of differences for 2 groups was determined by 2-sided t test and among 3 or more groups it was determined using 1-way ANOVA, followed by Sidak’s post hoc tests. *P < 0.05, **P < 0.01, ***P < 0.001.