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. 2018 Oct;59(4):467–478. doi: 10.1165/rcmb.2017-0129OC

Figure 6.

Figure 6.

Increased lung and circulating TCTP levels could contribute to the onset of experimental pulmonary arterial hypertension (PAH). Rats were administered vehicle or monocrotaline (MCT; 40 mg/kg). (A) Right ventricular systolic pressure (RVSP) and (B) right ventricular hypertrophy (RV/(LV+S)) were assessed in control (circles) and MCT-treated rats (squares) at weeks 1, 2, 3, and 4. One-way ANOVA; *P < 0.05, ***P < 0.001, ****P < 0.0001. Error bars represent mean ± SEM. (C) Representative immunoblot of TCTP expression in lungs isolated from controls at 1, 2, 3, and 4 weeks after MCT administration. Blots were reprobed for α-tubulin to ensure equal loading. (D) Densitometry of TCTP expression levels relative to α-tubulin. One-way ANOVA; *P < 0.05, **P < 0.01. Error bars represent mean ± SEM. (E) Plasma levels of TCTP measured by ELISA in control rats (circles) and at 1, 2, 3, and 4 weeks after MCT administration (squares). One-way ANOVA; **P < 0.01. Error bars represent median ± interquartile range.