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Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy

Mitofusin2 (Mfn2), a mitochondrial outer membrane protein serving primarily as a mitochondrial fusion protein, has multiple functions in regulating cell biological processes. Defects of Mfn2 were found in diabetes, obesity, and neurodegenerative diseases. In the present study, we found that knockdow...

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Detalles Bibliográficos
Autores principales: Ding, Yanhong, Gao, Han, Zhao, Lifang, Wang, Xian, Zheng, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363693/
https://www.ncbi.nlm.nih.gov/pubmed/25781899
http://dx.doi.org/10.1371/journal.pone.0121328
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author Ding, Yanhong
Gao, Han
Zhao, Lifang
Wang, Xian
Zheng, Ming
author_facet Ding, Yanhong
Gao, Han
Zhao, Lifang
Wang, Xian
Zheng, Ming
author_sort Ding, Yanhong
collection PubMed
description Mitofusin2 (Mfn2), a mitochondrial outer membrane protein serving primarily as a mitochondrial fusion protein, has multiple functions in regulating cell biological processes. Defects of Mfn2 were found in diabetes, obesity, and neurodegenerative diseases. In the present study, we found that knockdown of Mfn2 by shRNA led to impaired autophagic degradation, inhibited mitochondrial oxygen consumption rate and cell glycolysis, reduced ATP production, and suppressed cell proliferation. Inhibition of autophagic degradation mimicked Mfn2-deficiency mediated cell proliferation suppression, while enhancement of autophagosome maturation restored the suppressed cell proliferation by Mfn2-deficiency. Thus, our findings revealed the role of Mfn2 in regulating cell proliferation and mitochondrial metabolism, and shed new light on understanding the mechanisms of Mfn2 deficiency related diseases.
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spelling pubmed-43636932015-03-23 Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy Ding, Yanhong Gao, Han Zhao, Lifang Wang, Xian Zheng, Ming PLoS One Research Article Mitofusin2 (Mfn2), a mitochondrial outer membrane protein serving primarily as a mitochondrial fusion protein, has multiple functions in regulating cell biological processes. Defects of Mfn2 were found in diabetes, obesity, and neurodegenerative diseases. In the present study, we found that knockdown of Mfn2 by shRNA led to impaired autophagic degradation, inhibited mitochondrial oxygen consumption rate and cell glycolysis, reduced ATP production, and suppressed cell proliferation. Inhibition of autophagic degradation mimicked Mfn2-deficiency mediated cell proliferation suppression, while enhancement of autophagosome maturation restored the suppressed cell proliferation by Mfn2-deficiency. Thus, our findings revealed the role of Mfn2 in regulating cell proliferation and mitochondrial metabolism, and shed new light on understanding the mechanisms of Mfn2 deficiency related diseases. Public Library of Science 2015-03-17 /pmc/articles/PMC4363693/ /pubmed/25781899 http://dx.doi.org/10.1371/journal.pone.0121328 Text en © 2015 Ding et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Ding, Yanhong
Gao, Han
Zhao, Lifang
Wang, Xian
Zheng, Ming
Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy
title Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy
title_full Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy
title_fullStr Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy
title_full_unstemmed Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy
title_short Mitofusin 2-Deficiency Suppresses Cell Proliferation through Disturbance of Autophagy
title_sort mitofusin 2-deficiency suppresses cell proliferation through disturbance of autophagy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363693/
https://www.ncbi.nlm.nih.gov/pubmed/25781899
http://dx.doi.org/10.1371/journal.pone.0121328
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