Fig. 5: TXNDC5 is both essential and sufficient for HPF activation, proliferation, and ECM production. | Nature Communications

Fig. 5: TXNDC5 is both essential and sufficient for HPF activation, proliferation, and ECM production.

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

Fig. 5

Protein (n = 6 biologically independent samples per group) (a) and transcript (n = 6 biologically independent samples per group) (b) expression levels of COL1A1, fibronectin, elastin, periostin, and αSMA/ACTA2 were markedly increased in control (shScr) human pulmonary fibroblasts (HPF) following TGFβ1 (10 ng/ml) treatment. TGFβ1-induced upregulation of these fibrogenic proteins/genes was significantly attenuated in HPF with TXNDC5 depletion (shTXNDC5). c TGFβ1 treatment significantly increased the cellular proliferation activity in shScr-, but not in shTXNDC5-, transduced HPF (n = 24 biologically independent samples per group). ECM proteins (COL1A1 and fibronectin), markers for fibroblast activation (periostin and αSMA) (n = 9 biologically independent samples per group) (d) and fibroblast proliferation activity (n = 9 biologically independent samples per group) (e) were markedly increased in HPF transduced with TXNDC5 (TXNDC5 OE), compared with empty, expression vector (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, ctrl control, KD knockdown, OE overexpress).

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