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6. The role of SHP/REV-ERBα/CYP4A axis in the pathogenesis of alcohol-associated liver disease

Author

Yang, Zhihong, primary, Smalling, Rana V., additional, Huang, Yi, additional, Jiang, Yanchao, additional, Kusumanchi, Praveen, additional, Bogaert, Will, additional, Wang, Li, additional, Delker, Don A., additional, Skill, Nicholas J., additional, Han, Sen, additional, Zhang, Ting, additional, Ma, Jing, additional, Huda, Nazmul, additional, and Liangpunsakul, Suthat, additional

Published
2021
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8. Autophagy Ablation in Adipocytes Induces Insulin Resistance and Reveals Roles for Lipid Peroxide and Nrf2 Signaling in Adipose-Liver Crosstalk

Author

Cai, Jinjin, primary, Pires, Karla M., additional, Ferhat, Maroua, additional, Chaurasia, Bhagirath, additional, Buffolo, Márcio A., additional, Smalling, Rana, additional, Sargsyan, Ashot, additional, Atkinson, Donald L., additional, Summers, Scott A., additional, Graham, Timothy E., additional, and Boudina, Sihem, additional

Published
2018
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9. Hepatocytes Are the Principal Source of Circulating RBP4 in Mice

Author

Thompson, Spencer J., primary, Sargsyan, Ashot, additional, Lee, Seung-Ah, additional, Yuen, Jason J., additional, Cai, Jinjin, additional, Smalling, Rana, additional, Ghyselinck, Norbert, additional, Mark, Manuel, additional, Blaner, William S., additional, and Graham, Timothy E., additional

Published
2016
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11. Interactions Between Nuclear Receptor SHP and FOXA1 Maintain Oscillatory Homocysteine Homeostasis in Mice

Author

Tsuchiya, Hiroyuki, primary, da Costa, Kerry-Ann, additional, Lee, Sangmin, additional, Renga, Barbara, additional, Jaeschke, Hartmut, additional, Yang, Zhihong, additional, Orena, Stephen J., additional, Goedken, Michael J., additional, Zhang, Yuxia, additional, Kong, Bo, additional, Lebofsky, Margitta, additional, Rudraiah, Swetha, additional, Smalling, Rana, additional, Guo, Grace, additional, Fiorucci, Stefano, additional, Zeisel, Steven H., additional, and Wang, Li, additional

Published
2015
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12. Hepatocytes Are the Principal Source of Circulating RBP4 in Mice.

Author

Thompson, Spencer J., Sargsyan, Ashot, Seung-Ah Lee, Yuen, Jason J., Jinjin Cai, Smalling, Rana, Ghyselinck, Norbert, Mark, Manuel, Blaner, William S., Graham, Timothy E., Lee, Seung-Ah, and Cai, Jinjin

Subjects
RETINOL-binding proteins, LIVER cells, FAT cells, INSULIN resistance, AUTOCRINE mechanisms, MESSENGER RNA, GLUCOSE intolerance, ANIMALS, CARRIER proteins, EPITHELIAL cells, MICE, POLYMERASE chain reaction, RNA, WESTERN immunoblotting, REVERSE transcriptase polymerase chain reaction, GENOTYPES
Abstract

RBP4 is produced mainly by hepatocytes. In type 2 diabetes and obesity, circulating RBP4 is increased and may act systemically to cause insulin resistance and glucose intolerance. Observations that adipocyte RBP4 mRNA increases in parallel with circulating RBP4 in these conditions, whereas liver RBP4 mRNA does not, led to a widely held hypothesis that elevated circulating RBP4 is a direct result of increased production by adipocytes. To test this, we generated mice with hepatocyte-specific deletion of RBP4 (liver RBP4 knockout or LRKO mice). Adipose tissue RBP4 expression and secretion remained intact in LRKO mice and increased as expected in the setting of diet-induced insulin resistance. However, circulating RBP4 was undetectable in LRKO mice. We conclude that adipocyte RBP4 is not a significant source of circulating RBP4, even in the setting of insulin resistance. Adipocyte RBP4, therefore, may have a more important autocrine or paracrine function that is confined within the adipose tissue compartment. [ABSTRACT FROM AUTHOR]

Published
2017
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20. Genome-wide transcriptome analysis identifies novel gene signatures implicated in human chronic liver disease.

Author

Smalling RV, Delker DA, Zhang Y, Nieto N, McGuiness MS, Liu S, Friedman SL, Hagedorn CH, and Wang L

Subjects
Animals, Biopsy, Cluster Analysis, Computational Biology, Databases, Genetic, Disease Progression, Fatty Liver genetics, Female, Gene Expression Regulation, Gene Regulatory Networks, Genetic Predisposition to Disease, Genome-Wide Association Study, Hepatitis C, Chronic genetics, Humans, Immunohistochemistry, Liver Cirrhosis genetics, Liver Cirrhosis, Experimental genetics, Liver Diseases pathology, Liver Diseases, Alcoholic genetics, Male, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Non-alcoholic Fatty Liver Disease, Oligonucleotide Array Sequence Analysis, Phenotype, Rats, Rats, Sprague-Dawley, Receptors, Cytoplasmic and Nuclear deficiency, Receptors, Cytoplasmic and Nuclear genetics, Reproducibility of Results, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, RNA, Gene Expression Profiling methods, Genome, Human, Liver Diseases genetics, Receptors, Cytoplasmic and Nuclear metabolism
Abstract

The molecular mechanisms behind human liver disease progression to cirrhosis remain elusive. Nuclear receptor small heterodimer partner (SHP/Nr0b2) is a hepatic tumor suppressor and a critical regulator of liver function. SHP expression is diminished in human cirrhotic livers, suggesting a regulatory role in human liver diseases. The goal of this study was to identify novel SHP-regulated genes that are involved in the development and progression of chronic liver disease. To achieve this, we conducted the first comprehensive RNA sequencing (RNA-seq) analysis of Shp(-/-) mice, compared the results with human hepatitis C cirrhosis RNA-seq and nonalcoholic steatohepatitis (NASH) microarray datasets, and verified novel results in human liver biospecimens. This approach revealed new gene signatures associated with chronic liver disease and regulated by SHP. Several genes were selected for validation of physiological relevance based on their marked upregulation, novelty with regard to liver function, and involvement in gene pathways related to liver disease. These genes include peptidoglycan recognition protein 2, dual specific phosphatase-4, tetraspanin 4, thrombospondin 1, and SPARC-related modular calcium binding protein-2, which were validated by qPCR analysis of 126 human liver specimens, including steatosis, fibrosis, and NASH, alcohol and hepatitis C cirrhosis, and in mouse models of liver inflammation and injury. This RNA-seq analysis identifies new genes that are regulated by the nuclear receptor SHP and implicated in the molecular pathogenesis of human chronic liver diseases. The results provide valuable transcriptome information for characterizing mechanisms of these diseases.

Published
2013
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