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

Figure 6. TXNDC5-induced fibrogenic responses are mediated through TGFBR1.

Figure 6

(A) Immunoblots showed that treatment of TGF-β1 (10 ng/mL) induced upregulation of TGFBR1 and phosphorylation of SMAD3, whereas TGFBR2 was not affected. Knockdown of TXNDC5 abolished TGFBR1 upregulation and SMAD3 phosphorylation was induced by TGF-β1 in HKFs (n = 5–11). (B) Overexpression of TXNDC5 was sufficient to upregulate TGFBR1 and phospho-SMAD3 in HKFs (n = 5–6). (C) Knockdown of TGFBR1 abolished the upregulation of fibroblast activation markers and ECM proteins induced by TXNDC5 overexpression (n = 6–12). 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.