Growth differentiation factor 15 protects against the aging‐mediated systemic inflammatory response in humans and mice
Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunct...
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| Published in | Aging cell Vol. 19; no. 8; pp. e13195 - n/a |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.08.2020
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1474-9718 1474-9726 1474-9726 |
| DOI | 10.1111/acel.13195 |
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| Abstract | Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress‐induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro‐inflammatory cytokines in elderly subjects. Circulating levels of cell‐free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20‐month‐old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15‐deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL‐17 production in Th17 cells, GDF15 contributes to regulatory T‐cell‐mediated suppression of conventional T‐cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging‐mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice.
Aging‐induced GDF15 production is observed in humans and mice, which is positively correlated with systemic inflammation and mitochondrial stress. GDF15 deficiency promotes glucose intolerance as well as hepatic and adipose inflammation in old mice. GDF15 contributes to regulatory T cells‐mediated suppression of conventional T cell activation, but senescent T cells were resistant to regulatory T cells‐mediated suppression compared to conventional T cells. |
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| AbstractList | Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress‐induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of
GDF15
as well as pro‐inflammatory cytokines in elderly subjects. Circulating levels of cell‐free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic
Gdf15
expression. Mendelian randomization links reduced
GDF15
expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20‐month‐old mice. Aging also results in more severe liver injury and hepatic fat deposition in
Gdf15
‐deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL‐17 production in Th17 cells, GDF15 contributes to regulatory T‐cell‐mediated suppression of conventional T‐cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging‐mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice.
Aging‐induced GDF15 production is observed in humans and mice, which is positively correlated with systemic inflammation and mitochondrial stress. GDF15 deficiency promotes glucose intolerance as well as hepatic and adipose inflammation in old mice. GDF15 contributes to regulatory T cells‐mediated suppression of conventional T cell activation, but senescent T cells were resistant to regulatory T cells‐mediated suppression compared to conventional T cells. Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress‐induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro‐inflammatory cytokines in elderly subjects. Circulating levels of cell‐free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20‐month‐old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15‐deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL‐17 production in Th17 cells, GDF15 contributes to regulatory T‐cell‐mediated suppression of conventional T‐cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging‐mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice. Aging‐induced GDF15 production is observed in humans and mice, which is positively correlated with systemic inflammation and mitochondrial stress. GDF15 deficiency promotes glucose intolerance as well as hepatic and adipose inflammation in old mice. GDF15 contributes to regulatory T cells‐mediated suppression of conventional T cell activation, but senescent T cells were resistant to regulatory T cells‐mediated suppression compared to conventional T cells. Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress‐induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro‐inflammatory cytokines in elderly subjects. Circulating levels of cell‐free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20‐month‐old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15‐deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL‐17 production in Th17 cells, GDF15 contributes to regulatory T‐cell‐mediated suppression of conventional T‐cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging‐mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice. Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress‐induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro‐inflammatory cytokines in elderly subjects. Circulating levels of cell‐free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20‐month‐old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15 ‐deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL‐17 production in Th17 cells, GDF15 contributes to regulatory T‐cell‐mediated suppression of conventional T‐cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging‐mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice. Mitochondrial dysfunction is associated with aging-mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress-induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro-inflammatory cytokines in elderly subjects. Circulating levels of cell-free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20-month-old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15-deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL-17 production in Th17 cells, GDF15 contributes to regulatory T-cell-mediated suppression of conventional T-cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging-mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice.Mitochondrial dysfunction is associated with aging-mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress-induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro-inflammatory cytokines in elderly subjects. Circulating levels of cell-free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20-month-old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15-deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL-17 production in Th17 cells, GDF15 contributes to regulatory T-cell-mediated suppression of conventional T-cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging-mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice. |
| Audience | Academic |
| Author | Byun, Jin‐Seok Lee, Young‐Sun Goeminne, Ludger J. E. Kim, Seok‐Hwan Shong, Minho Jeon, Jae‐Han Yi, Hyon‐Seung Auwerx, Johan Nga, Ha Thi Ryu, Dongryeol Moon, Ji Sun Kim, Jung Tae Tian, Jing Wen Kang, Baeki E. Kang, Seul Gi |
| AuthorAffiliation | 9 Biomedical Institute for Convergence at SKKU (BICS) Sungkyunkwan University Suwon Republic of Korea 3 Department of Medical Science Chungnam National University School of Medicine Daejeon Republic of Korea 1 Research Center for Endocrine and Metabolic Diseases Chungnam National University Hospital Chungnam National University School of Medicine Daejeon Republic of Korea 8 Department of Internal Medicine School of Medicine Kyungpook National University Daegu Korea 10 Samsung Biomedical Research Institute Samsung Medical Center Seoul Republic of Korea 2 Laboratory of Integrative Systems Physiology École Polytechnique Fédérale de Lausanne (EPFL) Lausanne Switzerland 4 Department of Surgery Chungnam National University School of Medicine Daejeon Republic of Korea 7 Department of Internal Medicine Korea University College of Medicine Seoul Republic of Korea 6 Department of Oral Medicine School of Dentistry Kyungpook National University Daegu Republic of Korea 5 Department of Molecular Cell Biology |
| AuthorAffiliation_xml | – name: 5 Department of Molecular Cell Biology Sungkyunkwan University School of Medicine Suwon Republic of Korea – name: 7 Department of Internal Medicine Korea University College of Medicine Seoul Republic of Korea – name: 2 Laboratory of Integrative Systems Physiology École Polytechnique Fédérale de Lausanne (EPFL) Lausanne Switzerland – name: 6 Department of Oral Medicine School of Dentistry Kyungpook National University Daegu Republic of Korea – name: 4 Department of Surgery Chungnam National University School of Medicine Daejeon Republic of Korea – name: 3 Department of Medical Science Chungnam National University School of Medicine Daejeon Republic of Korea – name: 9 Biomedical Institute for Convergence at SKKU (BICS) Sungkyunkwan University Suwon Republic of Korea – name: 1 Research Center for Endocrine and Metabolic Diseases Chungnam National University Hospital Chungnam National University School of Medicine Daejeon Republic of Korea – name: 8 Department of Internal Medicine School of Medicine Kyungpook National University Daegu Korea – name: 10 Samsung Biomedical Research Institute Samsung Medical Center Seoul Republic of Korea |
| Author_xml | – sequence: 1 givenname: Ji Sun surname: Moon fullname: Moon, Ji Sun organization: Chungnam National University School of Medicine – sequence: 2 givenname: Ludger J. E. surname: Goeminne fullname: Goeminne, Ludger J. E. organization: École Polytechnique Fédérale de Lausanne (EPFL) – sequence: 3 givenname: Jung Tae surname: Kim fullname: Kim, Jung Tae organization: Chungnam National University School of Medicine – sequence: 4 givenname: Jing Wen surname: Tian fullname: Tian, Jing Wen organization: Chungnam National University School of Medicine – sequence: 5 givenname: Seok‐Hwan surname: Kim fullname: Kim, Seok‐Hwan organization: Chungnam National University School of Medicine – sequence: 6 givenname: Ha Thi surname: Nga fullname: Nga, Ha Thi organization: Chungnam National University School of Medicine – sequence: 7 givenname: Seul Gi surname: Kang fullname: Kang, Seul Gi organization: Chungnam National University School of Medicine – sequence: 8 givenname: Baeki E. surname: Kang fullname: Kang, Baeki E. organization: Sungkyunkwan University School of Medicine – sequence: 9 givenname: Jin‐Seok surname: Byun fullname: Byun, Jin‐Seok organization: Kyungpook National University – sequence: 10 givenname: Young‐Sun surname: Lee fullname: Lee, Young‐Sun organization: Korea University College of Medicine – sequence: 11 givenname: Jae‐Han surname: Jeon fullname: Jeon, Jae‐Han organization: Kyungpook National University – sequence: 12 givenname: Minho surname: Shong fullname: Shong, Minho organization: Chungnam National University School of Medicine – sequence: 13 givenname: Johan surname: Auwerx fullname: Auwerx, Johan organization: École Polytechnique Fédérale de Lausanne (EPFL) – sequence: 14 givenname: Dongryeol orcidid: 0000-0001-5905-6760 surname: Ryu fullname: Ryu, Dongryeol email: jmpbooks@cnu.ac.kr, freefall@skku.edu organization: Samsung Medical Center – sequence: 15 givenname: Hyon‐Seung orcidid: 0000-0002-3767-1954 surname: Yi fullname: Yi, Hyon‐Seung email: jmpbooks@cnu.ac.kr, freefall@skku.edu organization: Chungnam National University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32691494$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2020 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd 2020 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd. COPYRIGHT 2020 John Wiley & Sons, Inc. Copyright John Wiley & Sons, Inc. Aug 2020 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: 2020 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd – notice: 2020 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd. – notice: COPYRIGHT 2020 John Wiley & Sons, Inc. – notice: Copyright John Wiley & Sons, Inc. Aug 2020 – notice: 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | senescence aging inflammation T cell mitochondria |
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| License | Attribution 2020 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Snippet | Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and... Mitochondrial dysfunction is associated with aging-mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and... |
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| SubjectTerms | Adipose tissue Age Aging Aging - physiology Animals Body weight Cell activation Cell differentiation Chronic illnesses Cytokines Datasets Deoxyribonucleic acid Diabetes Diabetes mellitus (non-insulin dependent) Disease DNA Female Geriatrics Growth Growth Differentiation Factor 15 - metabolism Helper cells Homeostasis Humans Inflammation Inflammation - metabolism Inflammation - pathology Insulin Insulin resistance Kinases Liver Lymphocytes Lymphocytes T Male Mendelian Randomization Analysis Metabolic disorders Metabolism Mice Mice, Inbred C57BL Mice, Knockout mitochondria Mitochondrial DNA Older people Original Paper Phosphorylation Plasma senescence Serum levels T cell T cells Type 2 diabetes |
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| Title | Growth differentiation factor 15 protects against the aging‐mediated systemic inflammatory response in humans and mice |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.13195 https://www.ncbi.nlm.nih.gov/pubmed/32691494 https://www.proquest.com/docview/2434684783 https://www.proquest.com/docview/2448238212 https://www.proquest.com/docview/2425898312 https://pubmed.ncbi.nlm.nih.gov/PMC7431835 |
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