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Polo-like kinase 1 promotes pulmonary hypertension.
Chen, Rongrong; Wang, Hongfei; Zheng, Cuiting; Zhang, Xiyu; Li, Li; Wang, Shengwei; Chen, Hongyu; Duan, Jing; Zhou, Xian; Peng, Haiyong; Guo, Jing; Zhang, Anchen; Li, Feifei; Wang, Wang; Zhang, Yu; Wang, Jun; Wang, Chen; Meng, Yan; Du, Xinling; Zhang, Hongbing.
Afiliación
  • Chen R; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Wang H; Department of Cardiac Surgery, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • Zheng C; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Zhang X; Department of Pathology, Beijing Lab for Cardiovascular Precision Medicine, Key Laboratory of Medical Engineering for Cardiovascular Disease, Capital Medical University, Beijing, China.
  • Li L; Department of Pathology, Beijing Lab for Cardiovascular Precision Medicine, Key Laboratory of Medical Engineering for Cardiovascular Disease, Capital Medical University, Beijing, China.
  • Wang S; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Chen H; Department of Cardiac Surgery, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • Duan J; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Zhou X; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Peng H; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Guo J; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Zhang A; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Li F; Department of Cardiac Surgery, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • Wang W; Department of Cardiac Surgery, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • Zhang Y; Department of Physiology, Capital Medical University, Beijing, China.
  • Wang J; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Wang C; Department of Physiology, Capital Medical University, Beijing, China.
  • Meng Y; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
  • Du X; Department of Pathology, Beijing Lab for Cardiovascular Precision Medicine, Key Laboratory of Medical Engineering for Cardiovascular Disease, Capital Medical University, Beijing, China. yanmeng_my@ccmu.edu.cn.
  • Zhang H; Department of Cardiac Surgery, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. xinlingdu@hust.edu.cn.
Respir Res ; 24(1): 204, 2023 Aug 19.
Article en En | MEDLINE | ID: mdl-37598171
ABSTRACT

BACKGROUND:

Pulmonary hypertension (PH) is a lethal vascular disease with limited therapeutic options. The mechanistic connections between alveolar hypoxia and PH are not well understood. The aim of this study was to investigate the role of mitotic regulator Polo-like kinase 1 (PLK1) in PH development.

METHODS:

Mouse lungs along with human pulmonary arterial smooth muscle cells and endothelial cells were used to investigate the effects of hypoxia on PLK1. Hypoxia- or Sugen5416/hypoxia was applied to induce PH in mice. Plk1 heterozygous knockout mice and PLK1 inhibitors (BI 2536 and BI 6727)-treated mice were checked for the significance of PLK1 in the development of PH.

RESULTS:

Hypoxia stimulated PLK1 expression through induction of HIF1α and RELA. Mice with heterozygous deletion of Plk1 were partially resistant to hypoxia-induced PH. PLK1 inhibitors ameliorated PH in mice.

CONCLUSIONS:

Augmented PLK1 is essential for the development of PH and is a druggable target for PH.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Hipertensión Pulmonar Límite: Animals / Humans Idioma: En Revista: Respir Res Año: 2023 Tipo del documento: Article País de afiliación: China
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Hipertensión Pulmonar Límite: Animals / Humans Idioma: En Revista: Respir Res Año: 2023 Tipo del documento: Article País de afiliación: China