HIF-1α modulates β-catenin pathway to enhance the survival and angiogenesis of PBMSCs under hypoxia environment

Figure 7 Hypoxia-inducible factor-1α/β-catenin signaling promotes myocardial repair induced by peripheral blood mesenchymal stem cells therapy. A: Representative triphenyltetrazolium chloride staining of left ventricular basal, middle, and apex cross-sections in the sham, myocardial infarction, hypoxia-inducible factor-1α (HIF-1α) overexpression, β-catenin overexpression, HIF-1α knockdown plus β-catenin overexpression, or HIF-1α overexpression plus β-catenin knockdown-transfected peripheral blood mesenchymal stem cell (PBMSC) groups; B: Triphenyltetrazolium chloride-stained images were sectioned into transverse sections to assess the infarct size; C: Representative fluorescence microscopy images of tissue sections demonstrated the retention of enhanced green fluorescent protein (green)-labeled PBMSCs at the injection site at 90 days after transplantation. Representative double TUNEL staining for apoptotic PBMSCs in the infarcted tissues. 4’,6-diamidino-2-phenylindole was employed as a nuclear marker; D: Myocardial vessels were detected by immunofluorescence staining with an anti-CD31 antibody at 90 days after transplantation. Scale bar = 20 μm. All graphical data are presented as the means ± SEMs. ^bP < 0.01; ^cP < 0.001. n = 5 in each group. MI: Myocardial infarction; oeHIF-1α: Hypoxia-inducible factor-1α overexpression; shHIF-1α: Hypoxia-inducible factor-1α knockdown; oeβ-catenin: Β-catenin overexpression; shβ-catenin: Β-catenin knockdown; EGFP: Enhanced green fluorescent protein; DAPI: 4,6-diamino-2-phenylindole.