Figure 5
Upregulation of Wnt agonists and antagonists in myocardial tissues after myocardial infarction. (A) Diagram of the canonical Wnt/β-catenin signaling pathway, which is fine-tuned by the soluble Wnt ligands (green color) and Wnt inhibitors (red color) on the extracellular side of the plasma membrane. When a Wnt ligand binds to its plasma membrane receptor (purple color) and co-receptor (blue color), it leads to the inhibition of GSK-3β which is the key component of the β-catenin degradation complex; β-catenin will accumulate in the cytoplasm and then translocate into the nucleus where it, together with TCF/LEF, activate or inhibit the transcription of target genes. Abbreviations: GSK-3β, glycogen synthase kinase 3β; TCF/LEF, T-cell factor/lymphoid enhancer factor. (B) Detection of gene transcript levels from RNA samples extracted from heart tissues, which contained different cell types, such as cardiomyocytes (pink color), fibroblasts (brown color) and inflammatory cells (blue color). (C) and (D) qRT-PCR analyses of transcript levels of Wnt ligands (C) and Wnt inhibitors (D) in sham, 1-week post MI, and 8-week post MI infarct and border zone myocardium. n = 4–10 per group. *p < 0.05 vs. corresponding sham groups. “ns” means no significant difference between WT and KO groups. Data were analyzed by two-way ANOVA and Bonferroni post-hoc comparison.
