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Fig. 8 | Cardiovascular Diabetology

Fig. 8

From: Liraglutide preserves CD34+ stem cells from dysfunction Induced by high glucose exposure

Fig. 8

The GLP-1R antagonist EXE abolished ERK1/2 and AKT phosphorylation as well as the protective effects promoted by LIRA treatment. A Representative immunoblot of ERK1/2 and AKT phosphorylation after stimulation with LIRA 100 nM ± EXE 150 nM for 10 min. GAPDH was used as loading control. B, C Immunoblotting results presented as arbitrary units after normalization to the GAPDH protein levels. D Doubling time of CD34+ HSPCs cultured in NG, HG ± 50 nM and 100 nM ± EXE conditions (***p ≤ 0.001 HG vs NG; ** p ≤ 0.01 HG 100 LIRA vs HG; ** p ≤ 0.01 HG 100 LIRA + EXE vs NG; one-way ANOVA. E) Analysis by flow cytometry of CXCR4 expression in NG, HG ± 50 nM and 100 nM ± EXE CD34+ HSPCs (*p ≤ 0.05 HG vs NG; *p ≤ 0.05 HG 100 LIRA vs HG; *p ≤ 0.05 HG 100 LIRA + EXE vs NG; one-way ANOVA). EXE = exendin 9–39, HG = high glucose, LIRA = liraglutide, NG = normal glucose

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