Mitochondrial transplantation attenuates hypoxic pulmonary vasoconstriction
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Juan Zhou1, 2, 7,*, Jiwei Zhang3,*, Yankai Lu1, 2, 4,*, Songling Huang1, 2,*, Rui Xiao1, 2, Xianqin Zeng1, 2, Xiuyun Zhang1, 2, Jiansha Li2, 4, Tao Wang2, 5, Tongfei Li6, Liping Zhu1, 2, Qinghua Hu1, 2
1Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
2Key Laboratory of Pulmonary Diseases of Ministry of Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
3Department of Pathology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
4Department of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
5Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
6Department of Pathology, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China
7Current address: Department of Clinical Laboratory of Xuzhou Central Hospital, Xuzhou 221009, China
*These authors have contributed equally to this work
Qinghua Hu, e-mail: [email protected]
Keywords: hypoxia, reactive oxygen species, calcium signaling, pulmonary vasoconstriction, mitochondria
Received: January 07, 2016 Accepted: April 02, 2016 Published: April 21, 2016
Hypoxia triggers pulmonary vasoconstriction, however induces relaxation of systemic arteries such as femoral arteries. Mitochondria are functionally and structurally heterogeneous between different cell types. The aim of this study was to reveal whether mitochondrial heterogeneity controls the distinct responses of pulmonary versus systemic artery smooth muscle cells to hypoxia. Intact mitochondria were transplanted into Sprague-Dawley rat pulmonary artery smooth muscle cells in culture and pulmonary arteries in vitro. Mitochondria retained functional after transplantation. The cross transplantation of mitochondria between pulmonary and femoral artery smooth muscle cells reversed acute hypoxia-induced alterations in cell membrane potential, [Ca2+]i signaling in smooth muscle cells and constriction or relaxation of arteries. Furthermore, the high or low amount of reactive oxygen species generation from mitochondria and their divergent (dis-)abilities in activating extracellular Ca2+-sensing receptor in smooth muscle cells were found to cause cell membrane potential depolarization, [Ca2+]i elevation and constriction of pulmonary arteries versus cell membrane potential hyperpolarization, [Ca2+]i decline and relaxation of femoral arteries in response to hypoxia, respectively. Our findings suggest that mitochondria necessarily determine the behaviors of vascular smooth muscle cells in response to hypoxia.
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