SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics
Brown/beige adipocyte thermogenesis is a process that is important for energy balance. The thermogenesis of brown/beige adipocytes occurs in the mitochondria, which is modulated by the dynamic balance between mitochondrial fusion and fission. Mitophagy is also involved in mitochondrial dynamics. The...
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2022-06-01
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author | Se-Jun Park Dong-Hyun Shon Jae-Hyun Kim Yang-Hwan Ryu Yong Ko |
author_facet | Se-Jun Park Dong-Hyun Shon Jae-Hyun Kim Yang-Hwan Ryu Yong Ko |
author_sort | Se-Jun Park |
collection | DOAJ |
description | Brown/beige adipocyte thermogenesis is a process that is important for energy balance. The thermogenesis of brown/beige adipocytes occurs in the mitochondria, which is modulated by the dynamic balance between mitochondrial fusion and fission. Mitophagy is also involved in mitochondrial dynamics. The sorting and assembly machinery (SAM) complex protein, SAMM50, plays a key role in mitochondrial dynamics and quality control through regulating mitophagy. However, the roles of SAMM50 in the thermogenesis of beige adipocytes remain unknown. Thus, the objective of this study was to conduct functional analyses of SAMM50. The expression of mitochondrial fusion genes was repressed by SAMM50 knockdown but was not altered by SAMM50 overexpression. These results agreed with the distribution of the fluorescence-stained mitochondria and an mtDNA copy number. In contrast, the expression of mitochondrial fission genes showed an opposite outcome. As a result, suppression by the SAMM50 shRNA inhibited the expression of thermogenic genes (<i>UCP1</i>, <i>PPARGC1A</i>, <i>DIO2</i>, <i>ELOVL3</i>, <i>CIDEA</i>, and <i>CIDEC</i>) and mitochondrial-related genes (<i>CYCS</i>, <i>COX7A1</i>, <i>TFAM</i>, <i>CPT1B</i>, and <i>CPT2</i>). Conversely, SAMM50 overexpression promoted the expression of the thermogenic genes and mitochondrial genes. Thus, SAMM50 links the balance between the mitochondrial dynamics and thermogenesis of beige adipocytes. |
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spelling | doaj.art-b155aabb8f48469da820dfefb5c4aca42023-11-23T17:06:23ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-06-012312676410.3390/ijms23126764SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial DynamicsSe-Jun Park0Dong-Hyun Shon1Jae-Hyun Kim2Yang-Hwan Ryu3Yong Ko4Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul 02841, KoreaDivision of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul 02841, KoreaDivision of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul 02841, KoreaDivision of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul 02841, KoreaDivision of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul 02841, KoreaBrown/beige adipocyte thermogenesis is a process that is important for energy balance. The thermogenesis of brown/beige adipocytes occurs in the mitochondria, which is modulated by the dynamic balance between mitochondrial fusion and fission. Mitophagy is also involved in mitochondrial dynamics. The sorting and assembly machinery (SAM) complex protein, SAMM50, plays a key role in mitochondrial dynamics and quality control through regulating mitophagy. However, the roles of SAMM50 in the thermogenesis of beige adipocytes remain unknown. Thus, the objective of this study was to conduct functional analyses of SAMM50. The expression of mitochondrial fusion genes was repressed by SAMM50 knockdown but was not altered by SAMM50 overexpression. These results agreed with the distribution of the fluorescence-stained mitochondria and an mtDNA copy number. In contrast, the expression of mitochondrial fission genes showed an opposite outcome. As a result, suppression by the SAMM50 shRNA inhibited the expression of thermogenic genes (<i>UCP1</i>, <i>PPARGC1A</i>, <i>DIO2</i>, <i>ELOVL3</i>, <i>CIDEA</i>, and <i>CIDEC</i>) and mitochondrial-related genes (<i>CYCS</i>, <i>COX7A1</i>, <i>TFAM</i>, <i>CPT1B</i>, and <i>CPT2</i>). Conversely, SAMM50 overexpression promoted the expression of the thermogenic genes and mitochondrial genes. Thus, SAMM50 links the balance between the mitochondrial dynamics and thermogenesis of beige adipocytes.https://www.mdpi.com/1422-0067/23/12/6764adipose-derived stem cellsthermogenic adipocytesmitochondrial dynamicsobesitySAMM50UCP1 |
spellingShingle | Se-Jun Park Dong-Hyun Shon Jae-Hyun Kim Yang-Hwan Ryu Yong Ko SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics International Journal of Molecular Sciences adipose-derived stem cells thermogenic adipocytes mitochondrial dynamics obesity SAMM50 UCP1 |
title | SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics |
title_full | SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics |
title_fullStr | SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics |
title_full_unstemmed | SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics |
title_short | SAMM50 Regulates Thermogenesis of Beige Adipocytes Differentiated from Human Adipose-Derived Stem Cells by Balancing Mitochondrial Dynamics |
title_sort | samm50 regulates thermogenesis of beige adipocytes differentiated from human adipose derived stem cells by balancing mitochondrial dynamics |
topic | adipose-derived stem cells thermogenic adipocytes mitochondrial dynamics obesity SAMM50 UCP1 |
url | https://www.mdpi.com/1422-0067/23/12/6764 |
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