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

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© The Author(s) 2021

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Fig. 3. — Knockout of PKR inhibits SU5416/hypoxia-induced PH. (a–b) Right ventricle systolic pressure (RVSP) (b) and indices of RV weight (RV/LV+S) (c) in wild-type (WT) mice and PKR knockout mice after stimulation with SU5416/hypoxia (n = 6). (c) Photomicrographs of serial sections of peripheral mouse lung containing small arteries from wild-type mice and PKR knockout mice after stimulation with SU5416/hypoxia. Sections were immunostained for the α-SMA. Top scale bar = 200 µm. Bottom Scale Bar = 50 µm. (d) Quantitative assessment of pulmonary arterial muscularization in wild-type mice and PKR knockout mice after treatment with SU5416/hypoxia. **P < 0.01 by one-way ANOVA relative to wild-type mice treated with Su5416/hypoxia.