Journal
THERANOSTICS
Volume 6, Issue 8, Pages 1244-1260Publisher
IVYSPRING INT PUBL
DOI: 10.7150/thno.13804
Keywords
airway hyperresponsiveness; mitochondrial transplantation; cholinergic hyperactivity
Categories
Funding
- Natural Science Foundation of China [81170048, 81330001, 81400027, 30971162, 81470252, 81170049, 31270031, 31400990, 81572274, 30900545, 81370176]
- State Key Laboratory of Respiratory Disease [SKLRD2016OP001]
- Ministry of Education of China [NCET-12-0484]
- Health Department of Zhejiang Province [201342966]
- Natural Science Foundation of Zhejiang Province [LR12H01003]
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Increased cholinergic activity has been highlighted in the pathogenesis of airway hyperresponsiveness, and alternations of mitochondrial structure and function appear to be involved in many lung diseases including airway hyperresponsiveness. It is crucial to clarify the cause-effect association between mitochondrial dysfunction and cholinergic hyperactivity in the pathogenesis of airway hyperresponsiveness. Male SD rats and cultured airway epithelial cells were exposed to cigarette smoke plus lipopolysaccharide administration; mitochondria isolated from airway epithelium were delivered into epithelial cells in vitro and in vivo. Both the cigarette smoke plus lipopolysaccharide-induced cholinergic hyperactivity in vitro and the airway hyperresponsiveness to acetylcholine in vivo were reversed by the transplantation of exogenous mitochondria. The rescue effects of exogenous mitochondria were imitated by the elimination of excessive reactive oxygen species or blockage of muscarinic M-3 receptor, but inhibited by M receptor enhancer. Mitochondrial transplantation effectively attenuates cigarette smoke plus lipopolysaccharide-stimulated airway hyperresponsiveness through the inhibition of ROS-enhanced epithelial cholinergic hyperactivity.
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