Liver receptor homolog-1 (NR5A2) orchestrates hepatic inflammation and TNF-induced cell death
The nuclear receptor liver receptor homolog-1 (LRH-1) has been shown to promote apoptosis resistance in various tissues and disease contexts; however, its role in liver cell death remains unexplored. Hepatocyte-specific deletion of LRH-1 causes mild steatosis and inflammation but unexpectedly shield...
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Published in | Cell reports (Cambridge) Vol. 42; no. 12; p. 113513 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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26.12.2023
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Abstract | The nuclear receptor liver receptor homolog-1 (LRH-1) has been shown to promote apoptosis resistance in various tissues and disease contexts; however, its role in liver cell death remains unexplored. Hepatocyte-specific deletion of LRH-1 causes mild steatosis and inflammation but unexpectedly shields female mice from tumor necrosis factor (TNF)-induced hepatocyte apoptosis and associated hepatitis. LRH-1-deficient hepatocytes show markedly attenuated estrogen receptor alpha and elevated nuclear factor κB (NF-κB) activity, while LRH-1 overexpression inhibits NF-κB activity. This inhibition relies on direct physical interaction of LRH-1’s ligand-binding domain and the Rel homology domain of NF-κB subunit RelA. Mechanistically, increased transcription of anti-apoptotic NF-κB target genes and the proteasomal degradation of pro-apoptotic BCL-2 interacting mediator of cell death prevent mitochondrial apoptosis and ultimately protect mice from TNF-induced liver damage. Collectively, our study emphasizes LRH-1 as a critical, sex-dependent regulator of cell death and inflammation in the healthy and diseased liver.
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•Hepatic LRH-1 deletion causes mild liver steatosis, fibrosis, and inflammation•Female LRH-1-deficient mice are protected from TNF-induced liver damage•LRH-1 deletion reduces estrogen receptor activity and increases NF-κB activity•LRH-1 deletion-induced inflammation causes degradation of pro-apoptotic protein BIM
Lambrecht et al. report that liver-restricted deletion of LRH-1 sparks spontaneous inflammation but shields female mice from TNF-induced hepatitis. LRH-1 influences hepatic ERα and NF-κB activity, thereby impacting the apoptotic BCL-2 protein family. The study emphasizes LRH-1’s central and sex-related role in the hepatic transcription network. |
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AbstractList | The nuclear receptor liver receptor homolog-1 (LRH-1) has been shown to promote apoptosis resistance in various tissues and disease contexts; however, its role in liver cell death remains unexplored. Hepatocyte-specific deletion of LRH-1 causes mild steatosis and inflammation but unexpectedly shields female mice from tumor necrosis factor (TNF)-induced hepatocyte apoptosis and associated hepatitis. LRH-1-deficient hepatocytes show markedly attenuated estrogen receptor alpha and elevated nuclear factor κB (NF-κB) activity, while LRH-1 overexpression inhibits NF-κB activity. This inhibition relies on direct physical interaction of LRH-1's ligand-binding domain and the Rel homology domain of NF-κB subunit RelA. Mechanistically, increased transcription of anti-apoptotic NF-κB target genes and the proteasomal degradation of pro-apoptotic BCL-2 interacting mediator of cell death prevent mitochondrial apoptosis and ultimately protect mice from TNF-induced liver damage. Collectively, our study emphasizes LRH-1 as a critical, sex-dependent regulator of cell death and inflammation in the healthy and diseased liver. The nuclear receptor liver receptor homolog-1 (LRH-1) has been shown to promote apoptosis resistance in various tissues and disease contexts; however, its role in liver cell death remains unexplored. Hepatocyte-specific deletion of LRH-1 causes mild steatosis and inflammation but unexpectedly shields female mice from tumor necrosis factor (TNF)-induced hepatocyte apoptosis and associated hepatitis. LRH-1-deficient hepatocytes show markedly attenuated estrogen receptor alpha and elevated nuclear factor κB (NF-κB) activity, while LRH-1 overexpression inhibits NF-κB activity. This inhibition relies on direct physical interaction of LRH-1’s ligand-binding domain and the Rel homology domain of NF-κB subunit RelA. Mechanistically, increased transcription of anti-apoptotic NF-κB target genes and the proteasomal degradation of pro-apoptotic BCL-2 interacting mediator of cell death prevent mitochondrial apoptosis and ultimately protect mice from TNF-induced liver damage. Collectively, our study emphasizes LRH-1 as a critical, sex-dependent regulator of cell death and inflammation in the healthy and diseased liver. [Display omitted] •Hepatic LRH-1 deletion causes mild liver steatosis, fibrosis, and inflammation•Female LRH-1-deficient mice are protected from TNF-induced liver damage•LRH-1 deletion reduces estrogen receptor activity and increases NF-κB activity•LRH-1 deletion-induced inflammation causes degradation of pro-apoptotic protein BIM Lambrecht et al. report that liver-restricted deletion of LRH-1 sparks spontaneous inflammation but shields female mice from TNF-induced hepatitis. LRH-1 influences hepatic ERα and NF-κB activity, thereby impacting the apoptotic BCL-2 protein family. The study emphasizes LRH-1’s central and sex-related role in the hepatic transcription network. |
ArticleNumber | 113513 |
Author | Lambrecht, Rebekka Gloe, Vincent Plazzo, Anna Pia Franke, Barbara Schuetz, Karina San Phan, Truong Brunner, Thomas Delgado, M. Eugenia Mayans, Olga Fleming, Jennifer |
Author_xml | – sequence: 1 givenname: Rebekka surname: Lambrecht fullname: Lambrecht, Rebekka organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 2 givenname: M. Eugenia surname: Delgado fullname: Delgado, M. Eugenia organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 3 givenname: Vincent surname: Gloe fullname: Gloe, Vincent organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 4 givenname: Karina surname: Schuetz fullname: Schuetz, Karina organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 5 givenname: Anna Pia surname: Plazzo fullname: Plazzo, Anna Pia organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 6 givenname: Barbara surname: Franke fullname: Franke, Barbara organization: Biophysics and Structural Biology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 7 givenname: Truong surname: San Phan fullname: San Phan, Truong organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 8 givenname: Jennifer surname: Fleming fullname: Fleming, Jennifer organization: Biophysics and Structural Biology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 9 givenname: Olga surname: Mayans fullname: Mayans, Olga organization: Biophysics and Structural Biology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany – sequence: 10 givenname: Thomas orcidid: 0000-0002-1594-4712 surname: Brunner fullname: Brunner, Thomas email: thomas.brunner@uni-konstanz.de organization: Biochemical Pharmacology, Department of Biology, University of Konstanz, Universitätsstrasse 10, 78464 Konstanz, Germany |
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Keywords | CP: Immunology NF-κB LRH-1 liver ERα inflammation BIM apoptosis hepatitis TNF |
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