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. 2021 Sep 15;11(4):20458940211046156. doi: 10.1177/20458940211046156

Fig. 1.

Fig. 1.

PKR activation is elevated in the pulmonary vessels of experimental PH models. (a, b) Right ventricle systolic pressure (RVSP) (a) and indices of RV weight (RV/LV+S) (b) in rats given vehicle or MCT (60 mg/kg, i.p.) (n = 7). (c, d) Right ventricle systolic pressure (RVSP) measurements (c), indices of RV weight (RV/LV+S) (d) in vehicle and SU5416/hypoxia rats (n = 6). (e) Representative immunoblots and densitometric analysis of pulmonary artery PKR and p-PKR level in control and MCT rats (n = 3). (f) Representative immunoblots and densitometric analysis of pulmonary artery PKR and p-PKR level in control and SU5416/hypoxia rats (n = 3). (g) Photomicrographs of serial sections of peripheral rat lung containing small arteries from control animals and rats exposed to MCT rats. Sections were immunostained for the hematoxylin-eosin, PKR and p-PKR. Scale Bar = 25 µm. (h) Photomicrographs of serial sections of peripheral rat lung containing small arteries from control animals and SU5416/hypoxia rats. Sections were immunostained for the hematoxylin-eosin, PKR and p-PKR. Scale bar = 25 µm. (i) Representative immunoblots and densitometric analysis of PKR activation level was assessed in PAECs with TNF-α at 0, 10 and 20 ng/ml (n = 4). (j) Representative immunoblots and densitometric analysis of PKR activation level in PAECs under the treatment of TNF-α (20 ng/ml) for 0, 8 and 24 h (n = 4). *P < 0.05, **P < 0.01, ***P < 0.001, by one-way ANOVA relative to control groups.