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Transforming growth factor β regulates β-catenin expression in lung fibroblast through NF-κB dependent pathway.

Li J, Wang G, Sun X - Int. J. Mol. Med. (2014)

Bottom Line: Pretreatment of the NF-κB activation inhibitor attenuated the TGF-β‑induced expression of β-catenin and differentiation in human lung fibroblasts.Similarly, LPA induced β-catenin expression in human lung fibroblasts, and pre-treatment of the neutralized anti-TGF-β antibody attenuated the LPA‑induced expression of β-catenin and differentiation in human lung fibroblasts.The results suggested that β-catenin expression is upregulated in lung fibroblast during differentiation, and that TGF-β induced β-catenin expression in human lung fibroblasts through the activation of NF-κB.

View Article: PubMed Central - PubMed

Affiliation: Jinan Centre for Disease Control and Prevention, Jinan, Shandong 250001, P.R. China.

ABSTRACT
β-catenin contributes to the pathogenesis of lung fibrosis. However, the expression of β-catenin in fibroblasts under fibrotic conditions has not been studied. We investigated the expression of β-catenin in lung fibroblasts from bleomycin (BLM)‑challenged mice and human lung fibroblasts treated with transforming growth factor β (TGF-β) or lysophosphatidic acid (LPA) by western blot analysis. The result showed that the expression of β-catenin was significantly increased in lung fibrotic foci and lung fibroblasts from bleomycin‑challenged mice. TGF-β stimulated β-catenin expression and induced differentiation in human lung fibroblasts in vitro. Pretreatment of the NF-κB activation inhibitor attenuated the TGF-β‑induced expression of β-catenin and differentiation in human lung fibroblasts. Similarly, LPA induced β-catenin expression in human lung fibroblasts, and pre-treatment of the neutralized anti-TGF-β antibody attenuated the LPA‑induced expression of β-catenin and differentiation in human lung fibroblasts. The results suggested that β-catenin expression is upregulated in lung fibroblast during differentiation, and that TGF-β induced β-catenin expression in human lung fibroblasts through the activation of NF-κB.

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TGF-β induced the expression of β-catenin, FN and α-SMA in human lung fibroblasts. (a) Representative western blot and (b–d) quantification of the expression of (b) β-catenin, (c) FN and (d) α-SMA in human lung fibroblasts with or without TGF-β challenge. Data are expressed as means ± SEM of three independent experiments. *P<0.05 vs. cells without TGF-β challenge.
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f3-ijmm-34-05-1219: TGF-β induced the expression of β-catenin, FN and α-SMA in human lung fibroblasts. (a) Representative western blot and (b–d) quantification of the expression of (b) β-catenin, (c) FN and (d) α-SMA in human lung fibroblasts with or without TGF-β challenge. Data are expressed as means ± SEM of three independent experiments. *P<0.05 vs. cells without TGF-β challenge.

Mentions: TGF-β is a key factor for fibroblast differentiation, and plays critical roles in fibroblast differentiation. To determine whether the expression of β-catenin is correlated with TGF-β-induced activation and differentiation of lung fibroblasts, we assessed the expression of β-catenin in human lung fibroblasts challenged by TGF-β. Western blot analysis revealed that TGF-β challenge (5 ng/ml, 48 h) markedly increased the expression of β-catenin and fibroblast differentiation (Fig. 3a and d).


Transforming growth factor β regulates β-catenin expression in lung fibroblast through NF-κB dependent pathway.

Li J, Wang G, Sun X - Int. J. Mol. Med. (2014)

TGF-β induced the expression of β-catenin, FN and α-SMA in human lung fibroblasts. (a) Representative western blot and (b–d) quantification of the expression of (b) β-catenin, (c) FN and (d) α-SMA in human lung fibroblasts with or without TGF-β challenge. Data are expressed as means ± SEM of three independent experiments. *P<0.05 vs. cells without TGF-β challenge.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4199410&req=5

f3-ijmm-34-05-1219: TGF-β induced the expression of β-catenin, FN and α-SMA in human lung fibroblasts. (a) Representative western blot and (b–d) quantification of the expression of (b) β-catenin, (c) FN and (d) α-SMA in human lung fibroblasts with or without TGF-β challenge. Data are expressed as means ± SEM of three independent experiments. *P<0.05 vs. cells without TGF-β challenge.
Mentions: TGF-β is a key factor for fibroblast differentiation, and plays critical roles in fibroblast differentiation. To determine whether the expression of β-catenin is correlated with TGF-β-induced activation and differentiation of lung fibroblasts, we assessed the expression of β-catenin in human lung fibroblasts challenged by TGF-β. Western blot analysis revealed that TGF-β challenge (5 ng/ml, 48 h) markedly increased the expression of β-catenin and fibroblast differentiation (Fig. 3a and d).

Bottom Line: Pretreatment of the NF-κB activation inhibitor attenuated the TGF-β‑induced expression of β-catenin and differentiation in human lung fibroblasts.Similarly, LPA induced β-catenin expression in human lung fibroblasts, and pre-treatment of the neutralized anti-TGF-β antibody attenuated the LPA‑induced expression of β-catenin and differentiation in human lung fibroblasts.The results suggested that β-catenin expression is upregulated in lung fibroblast during differentiation, and that TGF-β induced β-catenin expression in human lung fibroblasts through the activation of NF-κB.

View Article: PubMed Central - PubMed

Affiliation: Jinan Centre for Disease Control and Prevention, Jinan, Shandong 250001, P.R. China.

ABSTRACT
β-catenin contributes to the pathogenesis of lung fibrosis. However, the expression of β-catenin in fibroblasts under fibrotic conditions has not been studied. We investigated the expression of β-catenin in lung fibroblasts from bleomycin (BLM)‑challenged mice and human lung fibroblasts treated with transforming growth factor β (TGF-β) or lysophosphatidic acid (LPA) by western blot analysis. The result showed that the expression of β-catenin was significantly increased in lung fibrotic foci and lung fibroblasts from bleomycin‑challenged mice. TGF-β stimulated β-catenin expression and induced differentiation in human lung fibroblasts in vitro. Pretreatment of the NF-κB activation inhibitor attenuated the TGF-β‑induced expression of β-catenin and differentiation in human lung fibroblasts. Similarly, LPA induced β-catenin expression in human lung fibroblasts, and pre-treatment of the neutralized anti-TGF-β antibody attenuated the LPA‑induced expression of β-catenin and differentiation in human lung fibroblasts. The results suggested that β-catenin expression is upregulated in lung fibroblast during differentiation, and that TGF-β induced β-catenin expression in human lung fibroblasts through the activation of NF-κB.

Show MeSH
Related in: MedlinePlus