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. 2022 Mar 23;13:810157. doi: 10.3389/fgene.2022.810157

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Copyright © 2022 Dong, Liu, Wu, Li, Wei, Wumaier, Zhang, Wang, Xia, Zhang, Yiminniyaze, Zhu, Li, Zhou, Zhang, Li, Lv and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Inhibition of MEK/ERK signaling protects rats against HPH. (A) A rat model of hypoxic pulmonary hypertension (HPH) was generated (n = 5 animals per group). Rats exposed to chronic hypoxia were treated with vehicle (DMSO) or 0.15 mg/kg or 0.3 mg/kg PD98059. (B) Rats in all groups were subjected to echocardiography and measurement of PAATand TAPSE. (C) After intubation for rats described in (A), RVSP was recorded, and the right ventricular hypertrophy ratio of RV/BW and RV/LV + S were calculated. (D) Hematoxylin and eosin staining of paraffin-fixed lung sections prepared from rats described in (A) was performed for morphological analysis of the pulmonary arteries. (E) A diagram showing that hypoxia-induced Mxi1-0 promotes PASMCs proliferation via MEK/ERK/c-Myc signaling in the context of HPH. Scale bar, 20 μm. Data are shown as means ± SDs. For statistical significance, ^***represents p < 0.001 compared to hypoxia. PAAT, pulmonary artery acceleration time; TAPSE, tricuspid annulusplain systolic excursion; RVSP, right ventricular systolic pressure; RV, right ventricle; BW, body weight; LV + S, left ventricle plus septum.