| MicroRNA expression profile in Lieber-DeCarli diet-induced alcoholic and methionine choline deficient diet-induced nonalcoholic steatohepatitis models in mice. | |
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MedLine Citation:
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PMID: 19572984 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Alcoholic and nonalcoholic steatohepatitis are leading causes of liver diseases worldwide. While of different etiology, these share common pathophysiological mechanisms and feature abnormal fat metabolism, inflammation and fibrosis. MicroRNAs (miRNA) are highly conserved noncoding RNAs that control gene expression at the post-transcriptional level either via the degradation of target mRNAs or the inhibition of translation. Each miRNA controls the expression of multiple targets; miRNAs have been linked to regulation of lipid metabolism and inflammation. METHODS: We fed Lieber-DeCarli alcohol or methionine-choline-deficient (MCD) diets to C57Bl6 and analyzed livers for histopathology, cytokines by ELISA, alanine aminotransferase (ALT) by biochemical assay, and microRNA profile by microarray. RESULTS: Both Lieber-DeCarli and MCD diets lead to development of liver steatosis, liver injury, indicated by increased ALT, and elevated levels of serum TNFalpha, suggesting that animal models portray the pathophysiological features of alcoholic and nonalcoholic fatty liver, respectively. We identified that Lieber-deCarli diet up-regulated 1% and down-regulated 1% of known miRNA; MCD diet up-regulated 3% and down-regulated 1% of known miRNA, compared to controls. Of miRNAs that changed expression levels, 5 miRNAs were common in alcoholic and nonalcoholic fatty livers: the expression of both miR-705 and miR-1224 was increased after Lieber-DeCarli or MCD diet feeding. In contrast, miR-182, miR-183, and miR-199a-3p were down-regulated in Lieber-deCarli feeding, while MCD diet lead to their up-regulation, compared to corresponding controls. CONCLUSIONS: Our findings indicate etiology-specific changes in miRNA expression profile during steatohepatitis models, which opens new avenues for research in the pathophysiology of alcoholic and nonalcoholic fatty liver disease. |
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Authors:
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Angela Dolganiuc; Jan Petrasek; Karen Kodys; Donna Catalano; Pranoti Mandrekar; Arumugam Velayudham; Gyongyi Szabo |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-07-01 |
Journal Detail:
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Title: Alcoholism, clinical and experimental research Volume: 33 ISSN: 1530-0277 ISO Abbreviation: Alcohol. Clin. Exp. Res. Publication Date: 2009 Oct |
Date Detail:
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Created Date: 2009-09-30 Completed Date: 2010-01-11 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7707242 Medline TA: Alcohol Clin Exp Res Country: England |
Other Details:
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Languages: eng Pagination: 1704-10 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605-2324, USA. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Central Nervous System Depressants / toxicity* Choline Deficiency / genetics*, pathology* Cytokines / blood Diet Ethanol / toxicity* Fatty Liver / genetics*, pathology Fatty Liver, Alcoholic / genetics*, pathology Female Inflammation / genetics, pathology Lipid Metabolism / genetics Liver / pathology Liver Function Tests Methionine / deficiency* Mice Mice, Inbred C57BL MicroRNAs / biosynthesis*, genetics* |
| Grant Support | |
ID/Acronym/Agency:
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1R01DK075635/DK/NIDDK NIH HHS; 5R01AA008577/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Central Nervous System Depressants; 0/Cytokines; 0/MicroRNAs; 63-68-3/Methionine; 64-17-5/Ethanol |
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