• Xiaoyu Fang, Min Xie, Xiansheng Liu, and Yuanzhou He.
• Department of Respiratory Diseases, Tongji Hospital, Key Lab of Pulmonary Diseases of Health Ministry, Key Site of National Clinical Research Center for Respiratory Disease, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430000, China.
• Biochem. Biophys. Res. Commun. 2021 Jun 11; 557: 40-47.

AbstractHypoxic pulmonary vascular remodeling is a pathological feature of pulmonary hypertension (PH). Our results showed that centromere-associated protein E (CENPE) expression in PH patients and hypoxia-induced PH rats was significantly higher than that in normal controls. In addition, CENPE deficiency significantly inhibited the development of pulmonary vascular remodeling and right ventricular hypertrophy. Moreover, knocking out CENPE effectively inhibited the proliferation and induced the apoptosis of primary pulmonary artery smooth muscle cells (PASMCs) in vivo. Furthermore, CENPE silencing by small interference significantly inhibited abnormal proliferation, apoptosis resistance, migration, and cell cycle arrest in hypoxia-induced PASMCs. Interestingly, we found that CENPE might exert its biological effect by targeting the transcription of CDK1 proteins.Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

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