Transferring Xenogenic Mitochondria Provides Neural Protection against Ischemic Stress in Ischemic Rat Brains

Transferring exogenous mitochondria has therapeutic effects on damaged heart, liver, and lung tissues. Whether this protective effect requires the symbiosis of exogenous mitochondria in host cells remains unknown. Here xenogenic mitochondria derived from a hamster cell line were applied to ischemic...

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Published in:	Cell transplantation 2016-05, Vol.25 (5), p.913-927
Main Authors:	Huang, Po-Jui, Kuo, Chi-Chung, Lee, Hsiu-Chin, Shen, Ching-I, Cheng, Fu-Chou, Wu, Shih-Fang, Chang, Jui-Chih, Pan, Hung-Chuan, Lin, Shinn-Zong, Liu, Chin-San, Su, Hong-Lin
Format:	Article
Language:	eng
Subjects:	Adenosine triphosphatase Animals Astrocytes Brain - pathology Brain Ischemia - pathology Brain Ischemia - therapy Cell death Cell Death - physiology Cell Line Cell Survival Central nervous system Cricetinae Electron transport Electron Transport - physiology Heart Infarction, Middle Cerebral Artery - pathology Infarction, Middle Cerebral Artery - therapy Injections, Intra-Arterial Internalization Ischemia Male Mitochondria Mitochondria - transplantation Motor task performance Neurons - cytology Neuroprotection - physiology Neuroprotective Agents - therapeutic use Rats Rats, Sprague-Dawley Symbiosis Transplantation, Heterologous
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Summary:	Transferring exogenous mitochondria has therapeutic effects on damaged heart, liver, and lung tissues. Whether this protective effect requires the symbiosis of exogenous mitochondria in host cells remains unknown. Here xenogenic mitochondria derived from a hamster cell line were applied to ischemic rat brains and rat primary cortical neurons. Isolated hamster mitochondria, either through local intracerebral or systemic intra-arterial injection, significantly restored the motor performance of brain-ischemic rats. The brain infarct area and neuronal cell death were both attenuated by the exogenous mitochondria. Although internalized mitochondria could be observed in neurons and astrocytes, the low efficacy of mitochondrial internalization could not completely account for the high rate of rescue of the treated neural cells. We further illustrated that disrupting electron transport or ATPase synthase in mitochondria significantly attenuated the protective effect, suggesting that intact respiratory activity is essential for the mitochondrial potency on neural protection. These results emphasize that nonsymbiotic extracellular mitochondria can provide an effective cell defense against acute injurious ischemic stress in the central nervous system.
ISSN:	0963-6897 1555-3892