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. Author manuscript; available in PMC: 2024 Mar 13.
Published in final edited form as: J Cell Physiol. 2021 Apr 30;236(11):7578–7590. doi: 10.1002/jcp.30401

FIGURE 1.

FIGURE 1

The ablation of TIGAR increases glycolysis and mitochondrial respiration in MAEC. (a)–(d), Glycolysis stress test and extracellular flux analysis of glycolysis, glycolytic capacity, and glycolytic reserve in the MAEC isolated from TIGAR KO and WT mice (n = 3-5). (e) Glucose uptake was not different between the WT and TIGAR KO MAECs (n = 5–7). (f)–(i) Mitochondrial stress test and extracellular flux analysis of mitochondrial basal and maximal respiration and ATP production in the MAEC isolated from TIGAR KO and WT mice (n = 5). ***p < .001, ****p < .0001. KO, knockout; MAECs, mouse aortic endothelial cells; TIGAR, TP53-induced glycolysis and apoptosis regulator; WT, wild type