Fig. 6: TXNDC5 modulates TGFBR1 expression in human lung fibroblasts and mouse lungs. | Nature Communications

Fig. 6: TXNDC5 modulates TGFBR1 expression in human lung fibroblasts and mouse lungs.

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

Fig. 6

a Immunoblots showed that TGFBR1, but not TGFBR2, was markedly upregulated in control HPF (shScr) following TGFβ1 treatment. TXNDC5 knockdown (shTXNDC5) prevented TGFBR1 upregulation induced by TGFβ1 treatment completely (n = 6 biologically independent samples per group). b Forced TXNDC5 expression led to marked upregulation of TGFBR1, but not TGFBR2, protein in HPF (n = 12 biologically independent samples per group). c TGFBR1 and COL1A1 proteins were both markedly upregulated in the lung tissues from WT, but not Txndc5−/−, mice 21 days following BLM treatment (WT sham n = 4, WT BLM n = 5, Txndc5−/− sham n = 3, Txndc5−/− BLM n = 5 biologically independent animals). d Representative IF staining and quantification (e) of TGFBR1 in Col1a1-GFPTg and Col1a1-GFPTg*Txndc5−/− mouse lungs with PBS (Sham) or BLM treatment on day 21 (n = 9 fields examined over 3 biologically independent animals per group). TGFBR1 was marked increased and showed strong co-localization with GFP-positive lung fibroblasts in BLM-treated mouse lungs. Global deletion of TXNDC5 prevented the upregulation of TGFBR1 in mouse lungs following BLM treatment (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, BLM bleomycin, TGFBR1 TGFβ receptor type 1, TGFBR2 TGFβ receptor type 2).

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