Fig. 1 | Nature Communications

Fig. 1

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

Fig. 1

Increased expression levels of ENO1 in hypertensive APAH patients and experimental PH animal lungs. a PASMC isolated from patients with IPAH or APAH and control donors were lysed and subjected to western blotting to measure the level of enolases. b Normalized quantification of proteins demonstrates the expression level of ENO1, ENO2, and ENO3 in PASMC isolated from patients with IPAH or APAH and control donors (n = 6 per group, *P = 0.0223). c mRNA levels of ENO1, ENO2, and ENO3 in PASMC from patients with PAH and the control donors. d Immunohistochemistry of ENO1 in lung tissue sections of patients with PAH and the control donors. Brown color indicates the staining of ENO1. Black arrows indicate the elevated of ENO1 staining in the PASMC layer of the vessels (scale bars, 100 μm). e Whole lung tissues were isolated from hypoxia-induced PH mice and western blotting was used to measure the level of enolases. f Normalized quantification of proteins demonstrates the expression level of enolases in the whole lung tissue of hypoxia-induced PH mice (n = 4 per group, *P = 0.0263). g mRNA levels of enolase in the whole lung tissue of hypoxia-induced PH mice (n = 3–6, P < 0.001). h Whole lung tissues were isolated from SuHx-induced PH rats and western blotting was used to measure the level of enolases. i Normalized quantification of protein demonstrates the expression level of enolases in the whole lung tissue of SuHx-induced PH rats (n = 4–5 per group, *P = 0.0447). j mRNA levels of enolase in the whole lung tissue of SuHx-induced PH rats (n = 3–6, *P = 0.0303). 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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