کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8840584 | 1614691 | 2018 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitoferrin-1 is Involved in the Progression of Alzheimer's Disease Through Targeting Mitochondrial Iron Metabolism in a Caenorhabditis elegans Model of Alzheimer's Disease
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کلمات کلیدی
TMRENGMAβROS - ROSβ-Amyloid - β-آمیلوئیدHydrogen peroxide - آب اکسیژنهtetramethylrhodamine ethyl ester - اتیل استر استرهای تترامتیل رودامینstandard deviation - انحراف معیارAlzheimer's disease - بیماری آلزایمرAlzheimer’s disease - بیماری آلزایمرOxidative stress - تنش اکسیداتیوnematode growth medium - رشد متوسط نماتدreverse transcription - رونویسی معکوسH2O2 - هیدروژن پراکسیدpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازCaenorhabditis elegans - کرم الگانس Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 385, 10 August 2018, Pages 90-101
Journal: Neuroscience - Volume 385, 10 August 2018, Pages 90-101
نویسندگان
Jiatao Huang, Sixi Chen, Li Hu, Huan Niu, Qianqian Sun, Wenna Li, Guoqian Tan, Jianghui Li, LongJin Jin, Jianxin Lyu, Huaibin Zhou,