Journal
NEUROSCIENCE
Volume 385, Issue -, Pages 90-101Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2018.06.011
Keywords
mitoferrin-1; mitochondrial iron metabolism; oxidative stress; beta-amyloid; Alzheimer's disease; Caenorhabditis elegans
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Funding
- Research Project of Zhejiang Province Education Department [Y201534276]
- Wenzhou Science & Technology Bureau [Y20170027]
- Zhejiang Provincial Natural Science Foundation of China [LY13H250002]
- Key Discipline of Zhejiang Province in Medical Technology
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In mammals, mitoferrin-1 and mitoferrin-2, two homologous proteins of the mitochondrial solute carrier family are required for iron delivery into mitochondria. However, there is only one kind, called W02B12 (mitoferrin-1 or mfn-1), in Caenorhabditis elegans and its regulatory mechanism is unknown. In this study, we used C. elegans strains CL2006 and GMC101 as models to investigate what role mitoferrin-1 played in Alzheimer's disease (AD). We found that knockdown of mitoferrin-1 by feeding-RNAi treatment extended lifespans of both strains of C. elegans. In addition, it reduced the paralysis rate in the GMC101 strain. These results suggest that mitoferrin-1 may be involved in the progression of Alzheimer's disease. Knockdown of mitoferrin-1 was seen to disturb mitochondrial morphology in the CB5600 strain. We tested whether knockdown of mitoferrin-1 could influence mitochondrial metabolism. Analysis of mitochondrial iron metabolism and mitochondrial ROS showed that knockdown of mitoferrin-1 could reduce mitochondrial iron content and reduce the level of mitochondrial ROS in the CL2006 and GMC101 strains. These results confirm that knockdown of mitoferrin-1 can slow the progress of disease in Alzheimer model of C. elegans and suggest that mitoferrin-1 plays a major role in mediating mitochondrial iron metabolism in this process. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.
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