Aging aggravates alcoholic liver injury and fibrosis in mice by downregulating sirtuin 1 expression
[Display omitted] Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury. C57BL/6...
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| Published in | Journal of hepatology Vol. 66; no. 3; pp. 601 - 609 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.03.2017
Elsevier Science Ltd |
| Subjects | |
| Online Access | Get full text |
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| Abstract | [Display omitted]
Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury.
C57BL/6 mice were subjected to short-term (10days) ethanol plus one binge or long-term (8weeks) ethanol plus multiple binges of ethanol. Liver injury and fibrosis were determined. Hepatic stellate cells (HSCs) were isolated and used in in vitro studies.
Middle-aged (12–14months) and old-aged (>16months) mice were more susceptible to liver injury, inflammation, and oxidative stress induced by short-term plus one binge or long-term plus multiple binges of ethanol feeding when compared to young (8–12weeks) mice. Long-term plus multiple binges of ethanol feeding induced greater liver fibrosis in middle-aged mice than that in young mice. Hepatic expression of sirtuin 1 (SIRT1) protein was downregulated in the middle-aged mice compared to young mice. Restoration of SIRT1 expression via the administration of adenovirus-SIRT1 vector ameliorated short-term plus binge ethanol-induced liver injury and fibrosis in middle-aged mice. HSCs isolated from middle-aged mice expressed lower levels of SIRT1 protein and were more susceptible to spontaneous activation in in vitro culture than those from young mice. Overexpression of SIRT1 reduced activation of HSCs from middle-aged mice in vitro with downregulation of PDGFR-α and c-Myc, while deletion of SIRT1 activated HSCs isolated from young mice in vitro. Finally, HSC-specific SIRT1 knockout mice were more susceptible to long-term chronic-plus-multiple binges of ethanol-induced liver fibrosis with upregulation of PDGFR-α expression.
Aging exacerbates ALD in mice through the downregulation of SIRT1 in hepatocytes and HSCs. Activation of SIRT1 may serve as a novel target for the treatment of ALD.
Aged mice are more susceptible to alcohol-induced liver injury and fibrosis, which is, at least in part, due to lower levels of sirtuin 1 protein in hepatocytes and hepatic stellate cells. Our findings suggest that sirtuin 1 activators may have beneficial effects for the treatment of alcoholic liver disease in aged patients. |
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| AbstractList | Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury.BACKGROUND & AIMSAging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury.C57BL/6 mice were subjected to short-term (10days) ethanol plus one binge or long-term (8weeks) ethanol plus multiple binges of ethanol. Liver injury and fibrosis were determined. Hepatic stellate cells (HSCs) were isolated and used in in vitro studies.METHODSC57BL/6 mice were subjected to short-term (10days) ethanol plus one binge or long-term (8weeks) ethanol plus multiple binges of ethanol. Liver injury and fibrosis were determined. Hepatic stellate cells (HSCs) were isolated and used in in vitro studies.Middle-aged (12-14months) and old-aged (>16months) mice were more susceptible to liver injury, inflammation, and oxidative stress induced by short-term plus one binge or long-term plus multiple binges of ethanol feeding when compared to young (8-12weeks) mice. Long-term plus multiple binges of ethanol feeding induced greater liver fibrosis in middle-aged mice than that in young mice. Hepatic expression of sirtuin 1 (SIRT1) protein was downregulated in the middle-aged mice compared to young mice. Restoration of SIRT1 expression via the administration of adenovirus-SIRT1 vector ameliorated short-term plus binge ethanol-induced liver injury and fibrosis in middle-aged mice. HSCs isolated from middle-aged mice expressed lower levels of SIRT1 protein and were more susceptible to spontaneous activation in in vitro culture than those from young mice. Overexpression of SIRT1 reduced activation of HSCs from middle-aged mice in vitro with downregulation of PDGFR-α and c-Myc, while deletion of SIRT1 activated HSCs isolated from young mice in vitro. Finally, HSC-specific SIRT1 knockout mice were more susceptible to long-term chronic-plus-multiple binges of ethanol-induced liver fibrosis with upregulation of PDGFR-α expression.RESULTSMiddle-aged (12-14months) and old-aged (>16months) mice were more susceptible to liver injury, inflammation, and oxidative stress induced by short-term plus one binge or long-term plus multiple binges of ethanol feeding when compared to young (8-12weeks) mice. Long-term plus multiple binges of ethanol feeding induced greater liver fibrosis in middle-aged mice than that in young mice. Hepatic expression of sirtuin 1 (SIRT1) protein was downregulated in the middle-aged mice compared to young mice. Restoration of SIRT1 expression via the administration of adenovirus-SIRT1 vector ameliorated short-term plus binge ethanol-induced liver injury and fibrosis in middle-aged mice. HSCs isolated from middle-aged mice expressed lower levels of SIRT1 protein and were more susceptible to spontaneous activation in in vitro culture than those from young mice. Overexpression of SIRT1 reduced activation of HSCs from middle-aged mice in vitro with downregulation of PDGFR-α and c-Myc, while deletion of SIRT1 activated HSCs isolated from young mice in vitro. Finally, HSC-specific SIRT1 knockout mice were more susceptible to long-term chronic-plus-multiple binges of ethanol-induced liver fibrosis with upregulation of PDGFR-α expression.Aging exacerbates ALD in mice through the downregulation of SIRT1 in hepatocytes and HSCs. Activation of SIRT1 may serve as a novel target for the treatment of ALD.CONCLUSIONSAging exacerbates ALD in mice through the downregulation of SIRT1 in hepatocytes and HSCs. Activation of SIRT1 may serve as a novel target for the treatment of ALD.Aged mice are more susceptible to alcohol-induced liver injury and fibrosis, which is, at least in part, due to lower levels of sirtuin 1 protein in hepatocytes and hepatic stellate cells. Our findings suggest that sirtuin 1 activators may have beneficial effects for the treatment of alcoholic liver disease in aged patients.LAY SUMMARYAged mice are more susceptible to alcohol-induced liver injury and fibrosis, which is, at least in part, due to lower levels of sirtuin 1 protein in hepatocytes and hepatic stellate cells. Our findings suggest that sirtuin 1 activators may have beneficial effects for the treatment of alcoholic liver disease in aged patients. [Display omitted] Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury. C57BL/6 mice were subjected to short-term (10days) ethanol plus one binge or long-term (8weeks) ethanol plus multiple binges of ethanol. Liver injury and fibrosis were determined. Hepatic stellate cells (HSCs) were isolated and used in in vitro studies. Middle-aged (12–14months) and old-aged (>16months) mice were more susceptible to liver injury, inflammation, and oxidative stress induced by short-term plus one binge or long-term plus multiple binges of ethanol feeding when compared to young (8–12weeks) mice. Long-term plus multiple binges of ethanol feeding induced greater liver fibrosis in middle-aged mice than that in young mice. Hepatic expression of sirtuin 1 (SIRT1) protein was downregulated in the middle-aged mice compared to young mice. Restoration of SIRT1 expression via the administration of adenovirus-SIRT1 vector ameliorated short-term plus binge ethanol-induced liver injury and fibrosis in middle-aged mice. HSCs isolated from middle-aged mice expressed lower levels of SIRT1 protein and were more susceptible to spontaneous activation in in vitro culture than those from young mice. Overexpression of SIRT1 reduced activation of HSCs from middle-aged mice in vitro with downregulation of PDGFR-α and c-Myc, while deletion of SIRT1 activated HSCs isolated from young mice in vitro. Finally, HSC-specific SIRT1 knockout mice were more susceptible to long-term chronic-plus-multiple binges of ethanol-induced liver fibrosis with upregulation of PDGFR-α expression. Aging exacerbates ALD in mice through the downregulation of SIRT1 in hepatocytes and HSCs. Activation of SIRT1 may serve as a novel target for the treatment of ALD. Aged mice are more susceptible to alcohol-induced liver injury and fibrosis, which is, at least in part, due to lower levels of sirtuin 1 protein in hepatocytes and hepatic stellate cells. Our findings suggest that sirtuin 1 activators may have beneficial effects for the treatment of alcoholic liver disease in aged patients. Background & Aims Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury. Methods C57BL/6 mice were subjected to short-term (10 days) ethanol plus one binge or long-term (8 weeks) ethanol plus multiple binges of ethanol. Liver injury and fibrosis were determined. Hepatic stellate cells (HSCs) were isolated and used in in vitro studies. Results Middle-aged (12–14 months) and old-aged (>16 months) mice were more susceptible to liver injury, inflammation, and oxidative stress induced by short-term plus one binge or long-term plus multiple binges of ethanol feeding when compared to young (8–12 weeks) mice. Long-term plus multiple binges of ethanol feeding induced greater liver fibrosis in middle-aged mice than that in young mice. Hepatic expression of sirtuin 1 (SIRT1) protein was downregulated in the middle-aged mice compared to young mice. Restoration of SIRT1 expression via the administration of adenovirus-SIRT1 vector ameliorated short-term plus binge ethanol-induced liver injury and fibrosis in middle-aged mice. HSCs isolated from middle-aged mice expressed lower levels of SIRT1 protein and were more susceptible to spontaneous activation in in vitro culture than those from young mice. Overexpression of SIRT1 reduced activation of HSCs from middle-aged mice in vitro with downregulation of PDGFR-α and c-Myc, while deletion of SIRT1 activated HSCs isolated from young mice in vitro. Finally, HSC-specific SIRT1 knockout mice were more susceptible to long-term chronic-plus-multiple binges of ethanol-induced liver fibrosis with upregulation of PDGFR-α expression. Conclusions Aging exacerbates ALD in mice through the downregulation of SIRT1 in hepatocytes and HSCs. Activation of SIRT1 may serve as a novel target for the treatment of ALD. Lay summary Aged mice are more susceptible to alcohol-induced liver injury and fibrosis, which is, at least in part, due to lower levels of sirtuin 1 protein in hepatocytes and hepatic stellate cells. Our findings suggest that sirtuin 1 activators may have beneficial effects for the treatment of alcoholic liver disease in aged patients. Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a chronic plus binge ethanol feeding model in mice to evaluate the effects of aging on alcohol-induced liver injury. C57BL/6 mice were subjected to short-term (10days) ethanol plus one binge or long-term (8weeks) ethanol plus multiple binges of ethanol. Liver injury and fibrosis were determined. Hepatic stellate cells (HSCs) were isolated and used in in vitro studies. Middle-aged (12-14months) and old-aged (>16months) mice were more susceptible to liver injury, inflammation, and oxidative stress induced by short-term plus one binge or long-term plus multiple binges of ethanol feeding when compared to young (8-12weeks) mice. Long-term plus multiple binges of ethanol feeding induced greater liver fibrosis in middle-aged mice than that in young mice. Hepatic expression of sirtuin 1 (SIRT1) protein was downregulated in the middle-aged mice compared to young mice. Restoration of SIRT1 expression via the administration of adenovirus-SIRT1 vector ameliorated short-term plus binge ethanol-induced liver injury and fibrosis in middle-aged mice. HSCs isolated from middle-aged mice expressed lower levels of SIRT1 protein and were more susceptible to spontaneous activation in in vitro culture than those from young mice. Overexpression of SIRT1 reduced activation of HSCs from middle-aged mice in vitro with downregulation of PDGFR-α and c-Myc, while deletion of SIRT1 activated HSCs isolated from young mice in vitro. Finally, HSC-specific SIRT1 knockout mice were more susceptible to long-term chronic-plus-multiple binges of ethanol-induced liver fibrosis with upregulation of PDGFR-α expression. Aging exacerbates ALD in mice through the downregulation of SIRT1 in hepatocytes and HSCs. Activation of SIRT1 may serve as a novel target for the treatment of ALD. Aged mice are more susceptible to alcohol-induced liver injury and fibrosis, which is, at least in part, due to lower levels of sirtuin 1 protein in hepatocytes and hepatic stellate cells. Our findings suggest that sirtuin 1 activators may have beneficial effects for the treatment of alcoholic liver disease in aged patients. Graphical abstract |
| Author | Varga, Zoltan V. Zhou, Zhou Pacher, Pal Xu, Ming-Jiang Yin, Shi Zang, Mengwei Mukhopadhyay, Partha Gao, Bin Feng, Dechun Wang, Hua Ramirez, Teresa Li, Yong-Mei |
| AuthorAffiliation | 1 Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD, 20892, USA 4 Barshop Institute for Longevity and Aging Studies, Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA 2 Department of Oncology, the First Affiliated Hospital, Institute for Liver Diseases of Anhui Medical University, Hefei, 230032, China 5 Laboratory of Cardiovascular Physiology and Tissue Injury, NIAAA, NIH, Bethesda, MD 20892, USA 3 Departmentof Geriatrics, Affiliated Provincial Hospital of Anhui Medical University |
| AuthorAffiliation_xml | – name: 4 Barshop Institute for Longevity and Aging Studies, Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA – name: 1 Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD, 20892, USA – name: 2 Department of Oncology, the First Affiliated Hospital, Institute for Liver Diseases of Anhui Medical University, Hefei, 230032, China – name: 5 Laboratory of Cardiovascular Physiology and Tissue Injury, NIAAA, NIH, Bethesda, MD 20892, USA – name: 3 Departmentof Geriatrics, Affiliated Provincial Hospital of Anhui Medical University |
| Author_xml | – sequence: 1 givenname: Teresa surname: Ramirez fullname: Ramirez, Teresa organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 2 givenname: Yong-Mei surname: Li fullname: Li, Yong-Mei organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 3 givenname: Shi surname: Yin fullname: Yin, Shi organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 4 givenname: Ming-Jiang surname: Xu fullname: Xu, Ming-Jiang organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 5 givenname: Dechun surname: Feng fullname: Feng, Dechun organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 6 givenname: Zhou surname: Zhou fullname: Zhou, Zhou organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 7 givenname: Mengwei surname: Zang fullname: Zang, Mengwei organization: Barshop Institute for Longevity and Aging Studies, Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, TX 78229, USA – sequence: 8 givenname: Partha surname: Mukhopadhyay fullname: Mukhopadhyay, Partha organization: Laboratory of Cardiovascular Physiology and Tissue Injury, NIAAA, NIH, Bethesda, MD 20892, USA – sequence: 9 givenname: Zoltan V. surname: Varga fullname: Varga, Zoltan V. organization: Laboratory of Cardiovascular Physiology and Tissue Injury, NIAAA, NIH, Bethesda, MD 20892, USA – sequence: 10 givenname: Pal surname: Pacher fullname: Pacher, Pal organization: Laboratory of Cardiovascular Physiology and Tissue Injury, NIAAA, NIH, Bethesda, MD 20892, USA – sequence: 11 givenname: Bin surname: Gao fullname: Gao, Bin email: bgao@mail.nih.gov organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA – sequence: 12 givenname: Hua surname: Wang fullname: Wang, Hua email: wanghua@ahmu.edu.cn organization: Laboratory of Liver Diseases, National Institutes of Health (NIH), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD 20892, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27871879$$D View this record in MEDLINE/PubMed |
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| Copyright | 2016 Published by Elsevier B.V. Copyright Elsevier Science Ltd. Mar 2017 |
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| Issue | 3 |
| Keywords | Middle-age Hepatic stellate cells (HSCs) Fatty liver Ethanol Steatohepatitis PDGFR-α |
| Language | English |
| License | Published by Elsevier B.V. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Dr. Teresa Ramirez, Dr. Yong-Mei Li and Dr. Shi Yin contributed equally to this work. |
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Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this... Graphical abstract Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this study was to use a... Background & Aims Aging is known to exacerbate the progression of alcoholic liver disease (ALD), but the underlying mechanisms remain obscure. The aim of this... |
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| SubjectTerms | Aging Aging - genetics Aging - metabolism Aging - pathology Alcohol Animals Binge Drinking c-Myc protein Cell culture Clonal deletion Cystic fibrosis Disease Models, Animal Down-Regulation Ethanol Fatty liver Female Fibrosis Gastroenterology and Hepatology Hepatic stellate cells (HSCs) Hepatic Stellate Cells - metabolism Hepatic Stellate Cells - pathology Hepatocytes Liver diseases Liver Diseases, Alcoholic - etiology Liver Diseases, Alcoholic - genetics Liver Diseases, Alcoholic - pathology Liver Regeneration Male Mice Mice, Inbred C57BL Mice, Knockout Middle-age Myc protein Oxidative Stress PDGFR-α SIRT1 protein Sirtuin 1 - deficiency Sirtuin 1 - genetics Steatohepatitis Stellate cells |
| Title | Aging aggravates alcoholic liver injury and fibrosis in mice by downregulating sirtuin 1 expression |
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