Cellular Location of HNF4α is Linked With Terminal Liver Failure in Humans
Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α‐based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decr...
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Published in | Hepatology communications Vol. 4; no. 6; pp. 859 - 875 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
01.06.2020
John Wiley and Sons Inc Wolters Kluwer Health/LWW |
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Abstract | Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α‐based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decrease as hepatic function deteriorates, and protein expression is found in the cytoplasm. These findings could explain impaired hepatic function in patients with degenerative liver disease. In this study, we analyzed HNF4α localization and the pathways involved in post‐translational modification of HNF4α in human hepatocytes from patients with decompensated liver function. RNA‐sequencing analysis revealed that AKT‐related pathways, specifically phospho‐AKT, is down‐regulated in cirrhotic hepatocytes from patients with terminal failure, in whom nuclear levels of HNF4α were significantly reduced, and cytoplasmic expression of HNF4α was increased. cMET was also significantly reduced in failing hepatocytes. Moreover, metabolic profiling showed a glycolytic phenotype in failing human hepatocytes. The contribution of cMET and phospho‐AKT to nuclear localization of HNF4α was confirmed using Spearman's rank correlation test and pathway analysis, and further correlated with hepatic dysfunction by principal component analysis. HNF4α acetylation, a posttranslational modification important for nuclear retention, was also significantly reduced in failing human hepatocytes when compared with normal controls. Conclusion: These results suggest that the alterations in the cMET‐AKT pathway directly correlate with HNF4α localization and level of hepatocyte dysfunction. This study suggests that manipulation of HNF4α and pathways involved in HNF4α posttranslational modification may restore hepatocyte function in patients with terminal liver failure.
Although drug induced liver injury (DILI) is a rare clinical event, it carries significant morbidity and mortality, leaving it as the leading cause of acute liver failure in the United States. It is one of the most challenging diagnoses encountered by gastroenterologists. DILI is also the most common single adverse event that has led to withdrawal of drugs from the marketplace, drug attrition and failure of implicated drugs to obtain FDA approval. The development of various drug injury networks have played a vital role in expanding our knowledge regarding drug, herbal and dietary supplement related liver injury. In this review, we discuss what defines liver injury, epidemiology of DILI, it's biochemical and pathologic patterns, and management. |
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AbstractList | Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α-based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decrease as hepatic function deteriorates, and protein expression is found in the cytoplasm. These findings could explain impaired hepatic function in patients with degenerative liver disease. In this study, we analyzed HNF4α localization and the pathways involved in post-translational modification of HNF4α in human hepatocytes from patients with decompensated liver function. RNA-sequencing analysis revealed that AKT-related pathways, specifically phospho-AKT, is down-regulated in cirrhotic hepatocytes from patients with terminal failure, in whom nuclear levels of HNF4α were significantly reduced, and cytoplasmic expression of HNF4α was increased. cMET was also significantly reduced in failing hepatocytes. Moreover, metabolic profiling showed a glycolytic phenotype in failing human hepatocytes. The contribution of cMET and phospho-AKT to nuclear localization of HNF4α was confirmed using Spearman's rank correlation test and pathway analysis, and further correlated with hepatic dysfunction by principal component analysis. HNF4α acetylation, a posttranslational modification important for nuclear retention, was also significantly reduced in failing human hepatocytes when compared with normal controls. Conclusion: These results suggest that the alterations in the cMET-AKT pathway directly correlate with HNF4α localization and level of hepatocyte dysfunction. This study suggests that manipulation of HNF4α and pathways involved in HNF4α posttranslational modification may restore hepatocyte function in patients with terminal liver failure. Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α-based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decrease as hepatic function deteriorates, and protein expression is found in the cytoplasm. These findings could explain impaired hepatic function in patients with degenerative liver disease. In this study, we analyzed HNF4α localization and the pathways involved in post-translational modification of HNF4α in human hepatocytes from patients with decompensated liver function. RNA-sequencing analysis revealed that AKT-related pathways, specifically phospho-AKT, is down-regulated in cirrhotic hepatocytes from patients with terminal failure, in whom nuclear levels of HNF4α were significantly reduced, and cytoplasmic expression of HNF4α was increased. cMET was also significantly reduced in failing hepatocytes. Moreover, metabolic profiling showed a glycolytic phenotype in failing human hepatocytes. The contribution of cMET and phospho-AKT to nuclear localization of HNF4α was confirmed using Spearman's rank correlation test and pathway analysis, and further correlated with hepatic dysfunction by principal component analysis. HNF4α acetylation, a posttranslational modification important for nuclear retention, was also significantly reduced in failing human hepatocytes when compared with normal controls. These results suggest that the alterations in the cMET-AKT pathway directly correlate with HNF4α localization and level of hepatocyte dysfunction. This study suggests that manipulation of HNF4α and pathways involved in HNF4α posttranslational modification may restore hepatocyte function in patients with terminal liver failure. Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α‐based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decrease as hepatic function deteriorates, and protein expression is found in the cytoplasm. These findings could explain impaired hepatic function in patients with degenerative liver disease. In this study, we analyzed HNF4α localization and the pathways involved in post‐translational modification of HNF4α in human hepatocytes from patients with decompensated liver function. RNA‐sequencing analysis revealed that AKT‐related pathways, specifically phospho‐AKT, is down‐regulated in cirrhotic hepatocytes from patients with terminal failure, in whom nuclear levels of HNF4α were significantly reduced, and cytoplasmic expression of HNF4α was increased. cMET was also significantly reduced in failing hepatocytes. Moreover, metabolic profiling showed a glycolytic phenotype in failing human hepatocytes. The contribution of cMET and phospho‐AKT to nuclear localization of HNF4α was confirmed using Spearman's rank correlation test and pathway analysis, and further correlated with hepatic dysfunction by principal component analysis. HNF4α acetylation, a posttranslational modification important for nuclear retention, was also significantly reduced in failing human hepatocytes when compared with normal controls. Conclusion: These results suggest that the alterations in the cMET‐AKT pathway directly correlate with HNF4α localization and level of hepatocyte dysfunction. This study suggests that manipulation of HNF4α and pathways involved in HNF4α posttranslational modification may restore hepatocyte function in patients with terminal liver failure. Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α‐based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decrease as hepatic function deteriorates, and protein expression is found in the cytoplasm. These findings could explain impaired hepatic function in patients with degenerative liver disease. In this study, we analyzed HNF4α localization and the pathways involved in post‐translational modification of HNF4α in human hepatocytes from patients with decompensated liver function. RNA‐sequencing analysis revealed that AKT‐related pathways, specifically phospho‐AKT, is down‐regulated in cirrhotic hepatocytes from patients with terminal failure, in whom nuclear levels of HNF4α were significantly reduced, and cytoplasmic expression of HNF4α was increased. cMET was also significantly reduced in failing hepatocytes. Moreover, metabolic profiling showed a glycolytic phenotype in failing human hepatocytes. The contribution of cMET and phospho‐AKT to nuclear localization of HNF4α was confirmed using Spearman's rank correlation test and pathway analysis, and further correlated with hepatic dysfunction by principal component analysis. HNF4α acetylation, a posttranslational modification important for nuclear retention, was also significantly reduced in failing human hepatocytes when compared with normal controls. Conclusion: These results suggest that the alterations in the cMET‐AKT pathway directly correlate with HNF4α localization and level of hepatocyte dysfunction. This study suggests that manipulation of HNF4α and pathways involved in HNF4α posttranslational modification may restore hepatocyte function in patients with terminal liver failure. Although drug induced liver injury (DILI) is a rare clinical event, it carries significant morbidity and mortality, leaving it as the leading cause of acute liver failure in the United States. It is one of the most challenging diagnoses encountered by gastroenterologists. DILI is also the most common single adverse event that has led to withdrawal of drugs from the marketplace, drug attrition and failure of implicated drugs to obtain FDA approval. The development of various drug injury networks have played a vital role in expanding our knowledge regarding drug, herbal and dietary supplement related liver injury. In this review, we discuss what defines liver injury, epidemiology of DILI, it's biochemical and pathologic patterns, and management. Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α‐based reprogramming corrects terminal liver failure in rats with chronic liver disease. In the livers of patients with advanced cirrhosis, HNF4α RNA expression levels decrease as hepatic function deteriorates, and protein expression is found in the cytoplasm. These findings could explain impaired hepatic function in patients with degenerative liver disease. In this study, we analyzed HNF4α localization and the pathways involved in post‐translational modification of HNF4α in human hepatocytes from patients with decompensated liver function. RNA‐sequencing analysis revealed that AKT‐related pathways, specifically phospho‐AKT, is down‐regulated in cirrhotic hepatocytes from patients with terminal failure, in whom nuclear levels of HNF4α were significantly reduced, and cytoplasmic expression of HNF4α was increased. cMET was also significantly reduced in failing hepatocytes. Moreover, metabolic profiling showed a glycolytic phenotype in failing human hepatocytes. The contribution of cMET and phospho‐AKT to nuclear localization of HNF4α was confirmed using Spearman's rank correlation test and pathway analysis, and further correlated with hepatic dysfunction by principal component analysis. HNF4α acetylation, a posttranslational modification important for nuclear retention, was also significantly reduced in failing human hepatocytes when compared with normal controls. Conclusion: These results suggest that the alterations in the cMET‐AKT pathway directly correlate with HNF4α localization and level of hepatocyte dysfunction. This study suggests that manipulation of HNF4α and pathways involved in HNF4α posttranslational modification may restore hepatocyte function in patients with terminal liver failure. Although drug induced liver injury (DILI) is a rare clinical event, it carries significant morbidity and mortality, leaving it as the leading cause of acute liver failure in the United States. It is one of the most challenging diagnoses encountered by gastroenterologists. DILI is also the most common single adverse event that has led to withdrawal of drugs from the marketplace, drug attrition and failure of implicated drugs to obtain FDA approval. The development of various drug injury networks have played a vital role in expanding our knowledge regarding drug, herbal and dietary supplement related liver injury. In this review, we discuss what defines liver injury, epidemiology of DILI, it's biochemical and pathologic patterns, and management. |
Author | Agarwal, Nandini Tafaleng, Edgar N. Collin de l'Hortet, Alexandra Paranjpe, Shirish Bell, Aaron Animasahun, Olamide Achreja, Abhinav Florentino, Rodrigo M. Arazov, Shohrat Hainer, Sarah J. Troy, Kris Fraunhoffer, Nicolas A. Nagrath, Deepak Takeishi, Kazuki Haep, Nils Guzman‐Lepe, Jorge Michalopoulos, George K. Banerjee, Swati Fox, Ira J. Soto‐Gutierrez, Alejandro Ostrowska, Alina Morita, Kazutoyo Mukherjee, Amitava |
AuthorAffiliation | 3 Facultad de Ciencias de la Salud Carrera de Medicina Universidad Maimónides Buenos Aires Argentina 9 School of Bioscience and Technology Vellore Institute of Technology Vellore India 5 Consejo Nacional de Investigaciones Científicas y Técnicas Buenos Aires Argentina 1 Department of Pathology University of Pittsburgh Pittsburgh PA 4 Centro de Estudios Farmacológicos y Botánicos‐CONICET Buenos Aires Argentina 6 Department of Surgery and Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan 10 Department of Biological Sciences University of Pittsburgh Pittsburgh PA 11 Department of Chemical Engineering and Rogel Cancer Center University of Michigan Ann Arbor MI 2 Department of Physiology and Biophysics Universidade Federal de Minas Gerais Belo Horizonte Brazil 7 Department of Surgery Children's Hospital of Pittsburgh of UPMC University of Pittsburgh Pittsburgh PA 8 Laboratory for Systems Biology of Human Diseases Department of Biomedical Engineering Biointerfaces Institute U |
AuthorAffiliation_xml | – name: 8 Laboratory for Systems Biology of Human Diseases Department of Biomedical Engineering Biointerfaces Institute University of Michigan Ann Arbor MI – name: 2 Department of Physiology and Biophysics Universidade Federal de Minas Gerais Belo Horizonte Brazil – name: 9 School of Bioscience and Technology Vellore Institute of Technology Vellore India – name: 10 Department of Biological Sciences University of Pittsburgh Pittsburgh PA – name: 4 Centro de Estudios Farmacológicos y Botánicos‐CONICET Buenos Aires Argentina – name: 6 Department of Surgery and Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan – name: 5 Consejo Nacional de Investigaciones Científicas y Técnicas Buenos Aires Argentina – name: 1 Department of Pathology University of Pittsburgh Pittsburgh PA – name: 11 Department of Chemical Engineering and Rogel Cancer Center University of Michigan Ann Arbor MI – name: 3 Facultad de Ciencias de la Salud Carrera de Medicina Universidad Maimónides Buenos Aires Argentina – name: 7 Department of Surgery Children's Hospital of Pittsburgh of UPMC University of Pittsburgh Pittsburgh PA |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32490322$$D View this record in MEDLINE/PubMed |
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Copyright | 2020 The Authors. Hepatology Communications published by Wiley Periodicals, Inc., on behalf of the American Association for the Study of Liver Diseases. 2020. This work is published under http://creativecommons.org/licenses/by-nc-nd/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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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Financial Disclosure: This work was supported by grants from NIH, DK099257, DK117881, DK119973, DK096990 and TR002383 to A.S.‐G. and CA227622, CA222251, & CA204969 to D.N. These authors contributed equally to this work. Potential conflict of interest: A.S.‐G., A.B. and I.J.F., are inventors on a patent application that describes the use of transcription factors to treat chronic liver failure (US20140249209). N.A.F., K.T., A.O., J.G.‐L., E.N.T., G.K.M., A.B., S.J.H., I.J.F. and A.S.‐G., are inventors on a provisional patent application related to methods to enhance hepatic functions in human failing livers (Application No.:62/915,765). A.S.‐G., J.G.‐L., K.T., A.C.‐D, Y.W. and I.J.F., are co‐founders and have a financial interest in Von Baer Wolff, Inc. a company focused on biofabrication of autologous human hepatocytes from stem cells technology and programming liver failure and their interests are managed by the Conflict of Interest Office at the University of Pittsburgh in accordance with their policies. |
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Snippet | Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α‐based reprogramming corrects... Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in hepatocyte function, and HNF4α-based reprogramming corrects... |
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StartPage | 859 |
SubjectTerms | Adenosine Alcohol Chromatography Kinases Laboratories Liver cirrhosis Liver diseases Localization Mass spectrometry Metabolites Original Principal components analysis Proteins Scientific imaging Transplants & implants |
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Title | Cellular Location of HNF4α is Linked With Terminal Liver Failure in Humans |
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