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Fig. 3 | Respiratory Research

Fig. 3

From: Transcriptomic analysis and validation reveal the pathogenesis and a novel biomarker of acute exacerbation of chronic obstructive pulmonary disease

Fig. 3

Validation of down-regulated WNT/β-catenin pathway in AECOPD. A WNT/β-catenin signaling pathway. The WNT ligands bind to the receptors, including the FZD family, the coreceptor LRP 5/6 and LGR4-6, downstream signaling molecules are activated, the destruction complex (Axin/ APC/ CK1/ GSK-3) is inhibited. The accumulation and translocation of dephosphorylated β-catenin to the nucleus drives the expression of T-cell factor/lymphoid enhancer-binding factor (TCF/LEF)-dependent genes. When there are no WNT ligands or fewer WNT ligands and receptors, the destruction complex is activated, causing phosphorylation of β-catenin to increase and eventually be degraded. Exogenous addition of lithium chloride can also inhibit the destruction complex, promotes β-catenin—mediated gene transcription. B The mRNA levels of WNT10b, WNT2, LRP6, LGR6, FZD4, CTNNB1, LEF1, FOSL1, and FRAT2 in the control group (n = 35), the stable COPD group (n = 27) and the AECOPD group (n = 30). Results are presented as relative mRNA level (mean ± SEM). Stable or Acute vs. Normal, *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. Acute vs. Stable, ###P < 0.001 by one-way ANOVA

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