Fig. 6 | Nature Communications

Fig. 6

From: Alpha-enolase regulates the malignant phenotype of pulmonary artery smooth muscle cells via the AMPK-Akt pathway

Fig. 6

Suppression of ENO1 prevents DMOG-mediated metabolic shift in PASMC. a Normal PASMCs were treated with 10 μM ENOblock for 12 h before the Seahorse assay. The OCR levels were measured using the mitochondrial stress test (n = 3–4 per group), and b the ECAR levels were measured using the glycolysis stress test in ENOblock-treated PASMCs (n = 3 per group). DMOG was used to mimic hypoxic conditions. The basal c and maximal d respiration level, basal e, and maximal f glycolytic level, and basal OCR/ECAR g were calculated accordingly. h The OCR levels were measured using the mitochondrial stress test (n = 3–4 per group) and the ECAR levels were measured using the glycolysis stress test in shENO1–PASMC (n = 3–4 per group). The basal j and maximal k respiration level, basal l, and maximal m glycolytic level, and basal OCR/ECAR n were calculated. *P < 0.05, **P < 0.01, n.s. = non-significance. Data represent the mean ± SEM. Student t test and one-way ANOVA were used to compare two and multiple groups. Bonferroni post-tests were carried out after ANOVA

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