Fig. 7: TXNDC5-induced pulmonary fibroblast activation and ECM production requires TGFBR1. | Nature Communications

Fig. 7: TXNDC5-induced pulmonary fibroblast activation and ECM production requires TGFBR1.

From: Fibroblast-enriched endoplasmic reticulum protein TXNDC5 promotes pulmonary fibrosis by augmenting TGFβ signaling through TGFBR1 stabilization

Fig. 7

a Forced expression of TXNDC5 in HPF led to increased SMAD3 phosphorylation, fibroblast activation (as evidenced by increased periostin levels) and ECM (COL1A1 and fibronectin) production, all of which were abolished completely by the treatment of LY364947 (10 μM for 48 h), a TGFBR1 kinase inhibitor (n = 6 biologically independent samples per group). b Knockdown of TGFBR1 reversed TXNDC5 overexpression-induced COL1A1, periostin, and αSMA expression (n = 4 biologically independent samples per group) (Data are presented as mean ± SEM, P value determined using two-tailed Mann–Whitney U test. Source data are provided as a Source Data file. n.s. non-significant, KD knockdown, OE overexpress, shTGFBR1 TGFBR1 knockdown with shRNA).

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