β‐Catenin regulation of farnesoid X receptor signaling and bile acid metabolism during murine cholestasis
Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β‐catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver‐specific β‐catenin knockout...
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| Published in | Hepatology (Baltimore, Md.) Vol. 67; no. 3; pp. 955 - 971 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Wolters Kluwer Health, Inc
01.03.2018
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β‐catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver‐specific β‐catenin knockout mice and wild‐type littermates were subjected to cholestatic injury through bile duct ligation or short‐term exposure to 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine diet. Intriguingly, knockout mice exhibit a dramatic protection from liver injury, fibrosis, and atypical ductular proliferation, which coincides with significantly decreased total hepatic bile acids (BAs). This led to the discovery of a role for β‐catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β‐catenin functions as both an inhibitor of nuclear translocation and a nuclear corepressor through formation of a physical complex with FXR. Loss of β‐catenin expedited FXR nuclear localization and FXR/retinoic X receptor alpha association, culminating in small heterodimer protein promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β‐catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β‐catenin expression during cholestatic injury reduces β‐catenin/FXR complex activation of FXR to decrease total BA and alleviate hepatic injury. Conclusion: We have identified an FXR/β‐catenin interaction whose modulation through β‐catenin suppression promotes FXR activation and decreases hepatic BAs, which may provide unique therapeutic opportunities in cholestatic liver diseases. (Hepatology 2018;67:955–971) |
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| AbstractList | Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation (ADP), and fibrosis. The Wnt/β-catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver-specific β-catenin knockout (KO) mice and wild-type (WT) littermates were subjected to cholestatic injury via bile duct ligation or short-term exposure to 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet. Intriguingly, KO exhibit a dramatic protection from liver injury, fibrosis, and ADP, which coincided with significantly decreased total hepatic bile acids (BA). This led to the discovery of a novel role for β-catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β-catenin functions as both an inhibitor of nuclear translocation and as a nuclear co-repressor through formation of a physical complex with FXR. Loss of β-catenin expedited FXR nuclear localization and FXR/RXRα association, culminating in small heterodimer protein (SHP) promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β-catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β-catenin expression during cholestatic injury reduces β-catenin/FXR complex, activates FXR to decrease total BA and alleviates hepatic injury. Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β‐catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver‐specific β‐catenin knockout mice and wild‐type littermates were subjected to cholestatic injury through bile duct ligation or short‐term exposure to 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine diet. Intriguingly, knockout mice exhibit a dramatic protection from liver injury, fibrosis, and atypical ductular proliferation, which coincides with significantly decreased total hepatic bile acids (BAs). This led to the discovery of a role for β‐catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β‐catenin functions as both an inhibitor of nuclear translocation and a nuclear corepressor through formation of a physical complex with FXR. Loss of β‐catenin expedited FXR nuclear localization and FXR/retinoic X receptor alpha association, culminating in small heterodimer protein promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β‐catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β‐catenin expression during cholestatic injury reduces β‐catenin/FXR complex activation of FXR to decrease total BA and alleviate hepatic injury. Conclusion: We have identified an FXR/β‐catenin interaction whose modulation through β‐catenin suppression promotes FXR activation and decreases hepatic BAs, which may provide unique therapeutic opportunities in cholestatic liver diseases. (H epatology 2018;67:955–971) Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β‐catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver‐specific β‐catenin knockout mice and wild‐type littermates were subjected to cholestatic injury through bile duct ligation or short‐term exposure to 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine diet. Intriguingly, knockout mice exhibit a dramatic protection from liver injury, fibrosis, and atypical ductular proliferation, which coincides with significantly decreased total hepatic bile acids (BAs). This led to the discovery of a role for β‐catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β‐catenin functions as both an inhibitor of nuclear translocation and a nuclear corepressor through formation of a physical complex with FXR. Loss of β‐catenin expedited FXR nuclear localization and FXR/retinoic X receptor alpha association, culminating in small heterodimer protein promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β‐catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β‐catenin expression during cholestatic injury reduces β‐catenin/FXR complex activation of FXR to decrease total BA and alleviate hepatic injury. Conclusion: We have identified an FXR/β‐catenin interaction whose modulation through β‐catenin suppression promotes FXR activation and decreases hepatic BAs, which may provide unique therapeutic opportunities in cholestatic liver diseases. (Hepatology 2018;67:955–971) Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β-catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver-specific β-catenin knockout mice and wild-type littermates were subjected to cholestatic injury through bile duct ligation or short-term exposure to 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet. Intriguingly, knockout mice exhibit a dramatic protection from liver injury, fibrosis, and atypical ductular proliferation, which coincides with significantly decreased total hepatic bile acids (BAs). This led to the discovery of a role for β-catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β-catenin functions as both an inhibitor of nuclear translocation and a nuclear corepressor through formation of a physical complex with FXR. Loss of β-catenin expedited FXR nuclear localization and FXR/retinoic X receptor alpha association, culminating in small heterodimer protein promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β-catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β-catenin expression during cholestatic injury reduces β-catenin/FXR complex activation of FXR to decrease total BA and alleviate hepatic injury. We have identified an FXR/β-catenin interaction whose modulation through β-catenin suppression promotes FXR activation and decreases hepatic BAs, which may provide unique therapeutic opportunities in cholestatic liver diseases. (Hepatology 2018;67:955-971). Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β-catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver-specific β-catenin knockout mice and wild-type littermates were subjected to cholestatic injury through bile duct ligation or short-term exposure to 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet. Intriguingly, knockout mice exhibit a dramatic protection from liver injury, fibrosis, and atypical ductular proliferation, which coincides with significantly decreased total hepatic bile acids (BAs). This led to the discovery of a role for β-catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β-catenin functions as both an inhibitor of nuclear translocation and a nuclear corepressor through formation of a physical complex with FXR. Loss of β-catenin expedited FXR nuclear localization and FXR/retinoic X receptor alpha association, culminating in small heterodimer protein promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β-catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β-catenin expression during cholestatic injury reduces β-catenin/FXR complex activation of FXR to decrease total BA and alleviate hepatic injury.Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The Wnt/β-catenin pathway plays a role in bile duct development, yet its role in cholestatic injury remains indeterminate. Liver-specific β-catenin knockout mice and wild-type littermates were subjected to cholestatic injury through bile duct ligation or short-term exposure to 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet. Intriguingly, knockout mice exhibit a dramatic protection from liver injury, fibrosis, and atypical ductular proliferation, which coincides with significantly decreased total hepatic bile acids (BAs). This led to the discovery of a role for β-catenin in regulating BA synthesis and transport through regulation of farnesoid X receptor (FXR) activation. We show that β-catenin functions as both an inhibitor of nuclear translocation and a nuclear corepressor through formation of a physical complex with FXR. Loss of β-catenin expedited FXR nuclear localization and FXR/retinoic X receptor alpha association, culminating in small heterodimer protein promoter occupancy and activation in response to BA or FXR agonist. Conversely, accumulation of β-catenin sequesters FXR, thus inhibiting its activation. Finally, exogenous suppression of β-catenin expression during cholestatic injury reduces β-catenin/FXR complex activation of FXR to decrease total BA and alleviate hepatic injury.We have identified an FXR/β-catenin interaction whose modulation through β-catenin suppression promotes FXR activation and decreases hepatic BAs, which may provide unique therapeutic opportunities in cholestatic liver diseases. (Hepatology 2018;67:955-971).CONCLUSIONWe have identified an FXR/β-catenin interaction whose modulation through β-catenin suppression promotes FXR activation and decreases hepatic BAs, which may provide unique therapeutic opportunities in cholestatic liver diseases. (Hepatology 2018;67:955-971). |
| Author | Ma, Xiaochao Thompson, Michael D. Cornuet, Pamela Moghe, Akshata Locker, Joseph Monga, Satdarshan P. Nejak‐Bowen, Kari Marino, Rebecca Abrams, Marc Tian, Jianmin Wang, Pengcheng |
| AuthorAffiliation | 2 Department of Medicine, University of Pittsburgh, Pittsburgh, PA 6 Dicerna Pharmaceuticals, Inc, Cambridge, MA 4 Pittsburgh Liver Research Center, University of Pittsburgh, Pittsburgh, PA 5 School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 1 Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 3 Department of Pathology, University of Pittsburgh, Pittsburgh, PA |
| AuthorAffiliation_xml | – name: 4 Pittsburgh Liver Research Center, University of Pittsburgh, Pittsburgh, PA – name: 5 School of Pharmacy, University of Pittsburgh, Pittsburgh, PA – name: 2 Department of Medicine, University of Pittsburgh, Pittsburgh, PA – name: 6 Dicerna Pharmaceuticals, Inc, Cambridge, MA – name: 1 Department of Pediatrics, Washington University School of Medicine, St. Louis, MO – name: 3 Department of Pathology, University of Pittsburgh, Pittsburgh, PA |
| Author_xml | – sequence: 1 givenname: Michael D. surname: Thompson fullname: Thompson, Michael D. organization: Washington University School of Medicine – sequence: 2 givenname: Akshata surname: Moghe fullname: Moghe, Akshata organization: University of Pittsburgh – sequence: 3 givenname: Pamela surname: Cornuet fullname: Cornuet, Pamela organization: University of Pittsburgh – sequence: 4 givenname: Rebecca surname: Marino fullname: Marino, Rebecca organization: University of Pittsburgh – sequence: 5 givenname: Jianmin surname: Tian fullname: Tian, Jianmin organization: University of Pittsburgh – sequence: 6 givenname: Pengcheng surname: Wang fullname: Wang, Pengcheng organization: University of Pittsburgh – sequence: 7 givenname: Xiaochao surname: Ma fullname: Ma, Xiaochao organization: University of Pittsburgh – sequence: 8 givenname: Marc surname: Abrams fullname: Abrams, Marc organization: Dicerna Pharmaceuticals, Inc – sequence: 9 givenname: Joseph surname: Locker fullname: Locker, Joseph organization: University of Pittsburgh – sequence: 10 givenname: Satdarshan P. surname: Monga fullname: Monga, Satdarshan P. email: smonga@pitt.edu organization: University of Pittsburgh – sequence: 11 givenname: Kari surname: Nejak‐Bowen fullname: Nejak‐Bowen, Kari email: knnst5@pitt.edu organization: University of Pittsburgh |
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| Notes | Supported by the National Institutes of Health (1R01DK62277 and 1R01DK100287 and Endowed Chair for Experimental Pathology, to S.P.S.M.; 1R01DK103775, to K.N.‐B.). See Editorial on Page 829 Potential conflict of interest: Dr. Monga consults and received grants from AbbVie and Dicerna. Dr. Abrams is employed by and owns stock in Dicerna. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| Snippet | Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation, and fibrosis. The... Cholestatic liver diseases result from impaired bile flow and are characterized by inflammation, atypical ductular proliferation (ADP), and fibrosis. The... |
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| SubjectTerms | Animals beta Catenin - metabolism Bile Bile acids Bile Acids and Salts - metabolism Bile ducts Catenin Cholestasis Cholestasis - metabolism Fibrosis Hepatology Liver - metabolism Liver - pathology Liver diseases Localization Mice Mice, Knockout Nuclear transport Receptors, Cytoplasmic and Nuclear - metabolism Rodents Signal Transduction Wnt protein |
| Title | β‐Catenin regulation of farnesoid X receptor signaling and bile acid metabolism during murine cholestasis |
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