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Lipopolysaccharide-induced proliferation and glycolysis in airway smooth muscle cells via activation of Drp1 |
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| Authors: | Lixin Zhang Cui Ma Xiaoying Wang Siyu He Qian Li Yutian Zhou Ying Liu Min Zhang Xiufeng Yu Xijuan Zhao Fei Li Da-ling Zhu |
| Institution: | 1. Department of Biopharmaceutical Sciences, Central Laboratory of Harbin Medical University (Daqing), Daqing, China
Department of Immunology, College of Medical Laboratory Science and Technology, Harbin Medical University (Daqing), Daqing, China Lixin Zhang and Cui Ma have contributed equally to this work.;2. Department of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Harbin, China;3. Department of Biopharmaceutical Sciences, Central Laboratory of Harbin Medical University (Daqing), Daqing, China Department of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Harbin, China;4. College of Pharmacy, Harbin of Commerce, Harbin, China;5. Department of Biopharmaceutical Sciences, Central Laboratory of Harbin Medical University (Daqing), Daqing, China Department of Immunology, College of Medical Laboratory Science and Technology, Harbin Medical University (Daqing), Daqing, China;6. Department of Biopharmaceutical Sciences, Central Laboratory of Harbin Medical University (Daqing), Daqing, China;7. College of Basic Medicine, Harbin Medical University (Daqing), Daqing, China |
| Abstract: | Abnormal airway smooth muscle cells (ASMCs) proliferation is an important pathological process in airway remodeling contributes to increased mortality in asthma. Mitochondrial dynamics and metabolism have a central role in the maintenance of the cell function. In this study, lipopolysaccharide (LPS)-induced ASMCs proliferative model was used to investigate the effect of mitochondria on the proliferation of ASMCs and the possible mechanism. We used cell and molecular biology to determine the effect of dynamin-related protein 1 (Drp1) on LPS-mediated ASMCs cell cycle progression and glycolysis. The major findings of the current study are as follows: LPS promoted an increased mitochondrial fission and phosphorylation of Drp1 at Ser616 (p-Drp1 Ser616). LPS-induced ASMCs proliferation and cell cycle progression, which was significantly inhibited application of Drp1 RNA interfering. Glycolysis inhibitor 2-deoxyglucose (2-DG) depressed ASMCs proliferative process induced by LPS stimulation. LPS caused mitochondrial metabolism disorders and aerobic glycolysis in a dependent on Drp1 activation. These results indicated that Drp1 may function as a key factor in asthma airway remodeling by mediating ASMC proliferation and cell cycle acceleration through an effect on mitochondrial metabolic disturbance. |
| Keywords: | DRP1 glycolysis LPS mitochondria proliferation |