Mannose Phosphate Isomerase and Mannose Regulate Hepatic Stellate Cell Activation and Fibrosis in Zebrafish and Humans
The growing burden of liver fibrosis and lack of effective antifibrotic therapies highlight the need for identification of pathways and complementary model systems of hepatic fibrosis. A rare, monogenic disorder in which children with mutations in mannose phosphate isomerase (MPI) develop liver fibr...
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| Published in | Hepatology (Baltimore, Md.) Vol. 70; no. 6; pp. 2107 - 2122 |
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| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Wiley Subscription Services, Inc
01.12.2019
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| Abstract | The growing burden of liver fibrosis and lack of effective antifibrotic therapies highlight the need for identification of pathways and complementary model systems of hepatic fibrosis. A rare, monogenic disorder in which children with mutations in mannose phosphate isomerase (MPI) develop liver fibrosis led us to explore the function of MPI and mannose metabolism in liver development and adult liver diseases. Herein, analyses of transcriptomic data from three human liver cohorts demonstrate that MPI gene expression is down‐regulated proportionate to fibrosis in chronic liver diseases, including nonalcoholic fatty liver disease and hepatitis B virus. Depletion of MPI in zebrafish liver in vivo and in human hepatic stellate cell (HSC) lines in culture activates fibrotic responses, indicating that loss of MPI promotes HSC activation. We further demonstrate that mannose supplementation can attenuate HSC activation, leading to reduced fibrogenic activation in zebrafish, culture‐activated HSCs, and in ethanol‐activated HSCs. Conclusion: These data indicate the prospect that modulation of mannose metabolism pathways could reduce HSC activation and improve hepatic fibrosis. |
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| AbstractList | The growing burden of liver fibrosis and lack of effective antifibrotic therapies highlight the need for identification of pathways and complementary model systems of hepatic fibrosis. A rare, monogenic disorder in which children with mutations in mannose phosphate isomerase (MPI) develop liver fibrosis led us to explore the function of MPI and mannose metabolism in liver development and adult liver diseases. Herein, analyses of transcriptomic data from three human liver cohorts demonstrate that MPI gene expression is down‐regulated proportionate to fibrosis in chronic liver diseases, including nonalcoholic fatty liver disease and hepatitis B virus. Depletion of MPI in zebrafish liver in vivo and in human hepatic stellate cell (HSC) lines in culture activates fibrotic responses, indicating that loss of MPI promotes HSC activation. We further demonstrate that mannose supplementation can attenuate HSC activation, leading to reduced fibrogenic activation in zebrafish, culture‐activated HSCs, and in ethanol‐activated HSCs. Conclusion: These data indicate the prospect that modulation of mannose metabolism pathways could reduce HSC activation and improve hepatic fibrosis. The growing burden of liver fibrosis and lack of effective antifibrotic therapies highlight the need for identification of pathways and complementary model systems of hepatic fibrosis. A rare, monogenic disorder in which children with mutations in mannose phosphate isomerase (MPI) develop liver fibrosis led us to explore the function of MPI and mannose metabolism in liver development and adult liver diseases. Herein, analyses of transcriptomic data from three human liver cohorts demonstrate that MPI gene expression is down-regulated proportionate to fibrosis in chronic liver diseases, including nonalcoholic fatty liver disease and hepatitis B virus. Depletion of MPI in zebrafish liver in vivo and in human hepatic stellate cell (HSC) lines in culture activates fibrotic responses, indicating that loss of MPI promotes HSC activation. We further demonstrate that mannose supplementation can attenuate HSC activation, leading to reduced fibrogenic activation in zebrafish, culture-activated HSCs, and in ethanol-activated HSCs. |
| Author | Huang, Kuan‐lin DeRossi, Charles Lee, Youngmin A. Morrison, Joshua Fiel, M. Isabel Sakaguchi, Takuya F. Villanueva, Augusto Zhang, Changwen Sakarin, Isabel Bambino, Kathryn Ellis, Jillian L. Villacorta‐Martin, Carlos Chu, Jaime Ybanez, Maria Yin, Chunyue Friedman, Scott L. |
| AuthorAffiliation | 4 Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 5 Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 7 Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 8 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 9 Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 1 Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY 2 Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY 6 Laboratory of RNA Molecular Biology, Rockefeller University, New York, NY 3 Center for Regenerative Medicine, Boston University and Boston Medical Center, Boston, MA |
| AuthorAffiliation_xml | – name: 7 Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY – name: 5 Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY – name: 2 Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY – name: 4 Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: 9 Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH – name: 1 Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY – name: 6 Laboratory of RNA Molecular Biology, Rockefeller University, New York, NY – name: 3 Center for Regenerative Medicine, Boston University and Boston Medical Center, Boston, MA – name: 8 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY |
| Author_xml | – sequence: 1 givenname: Charles orcidid: 0000-0001-5267-6553 surname: DeRossi fullname: DeRossi, Charles organization: Icahn School of Medicine at Mount Sinai – sequence: 2 givenname: Kathryn surname: Bambino fullname: Bambino, Kathryn organization: Icahn School of Medicine at Mount Sinai – sequence: 3 givenname: Joshua surname: Morrison fullname: Morrison, Joshua organization: Icahn School of Medicine at Mount Sinai – sequence: 4 givenname: Isabel surname: Sakarin fullname: Sakarin, Isabel organization: Icahn School of Medicine at Mount Sinai – sequence: 5 givenname: Carlos surname: Villacorta‐Martin fullname: Villacorta‐Martin, Carlos organization: Boston University and Boston Medical Center – sequence: 6 givenname: Changwen surname: Zhang fullname: Zhang, Changwen organization: Cincinnati Children’s Hospital Medical Center – sequence: 7 givenname: Jillian L. surname: Ellis fullname: Ellis, Jillian L. organization: Cincinnati Children’s Hospital Medical Center – sequence: 8 givenname: M. Isabel surname: Fiel fullname: Fiel, M. Isabel organization: Icahn School of Medicine at Mount Sinai – sequence: 9 givenname: Maria surname: Ybanez fullname: Ybanez, Maria organization: Icahn School of Medicine at Mount Sinai – sequence: 10 givenname: Youngmin A. surname: Lee fullname: Lee, Youngmin A. organization: Rockefeller University – sequence: 11 givenname: Kuan‐lin surname: Huang fullname: Huang, Kuan‐lin organization: Icahn School of Medicine at Mount Sinai – sequence: 12 givenname: Chunyue orcidid: 0000-0002-3784-6363 surname: Yin fullname: Yin, Chunyue organization: Cincinnati Children’s Hospital Medical Center – sequence: 13 givenname: Takuya F. surname: Sakaguchi fullname: Sakaguchi, Takuya F. organization: Lerner Research Institute, Cleveland Clinic Foundation – sequence: 14 givenname: Scott L. surname: Friedman fullname: Friedman, Scott L. organization: Icahn School of Medicine at Mount Sinai – sequence: 15 givenname: Augusto surname: Villanueva fullname: Villanueva, Augusto organization: Icahn School of Medicine at Mount Sinai – sequence: 16 givenname: Jaime surname: Chu fullname: Chu, Jaime email: jaime.chu@mssm.edu organization: Icahn School of Medicine at Mount Sinai |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31016744$$D View this record in MEDLINE/PubMed |
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| Copyright | 2019 by the American Association for the Study of Liver Diseases. |
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| SubjectTerms | Animals Cell activation Cell culture Cells, Cultured Danio rerio Ethanol Fatty liver Fibrosis Gene expression Glycosylation Hepatic Stellate Cells - physiology Hepatitis B Hepatology Humans Liver Cirrhosis - etiology Liver diseases Male Mannose Mannose - pharmacology Mannose-6-Phosphate Isomerase - physiology Metabolism Mpi gene Platelet-Derived Growth Factor - physiology Signal Transduction - physiology Supplements Zebrafish |
| Title | Mannose Phosphate Isomerase and Mannose Regulate Hepatic Stellate Cell Activation and Fibrosis in Zebrafish and Humans |
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