miR-122 regulation of lipid metabolism revealed by in vivo antisense targeting
Open accessAbstract
Current understanding of microRNA (miRNA) biology is limited, and antisense oligonucleotide (ASO) inhibition of miRNAs is a powerful technique for their functionalization. To uncover the role of the liver-specific miR-122 in the adult liver, we inhibited it in mice with a 2'-O-methoxyethyl phosphorothioate ASO. miR-122 inhibition in normal mice resulted in reduced plasma cholesterol levels, increased hepatic fatty-acid oxidation, and a decrease in hepatic fatty-acid and cholesterol synthesis rates. Activation of the central metabolic sensor AMPK was also increased. miR-122 inhibition in a diet-induced obesity mouse model resulted in decreased plasma cholesterol levels and a significant improvement in liver steatosis, accompanied by reductions in several lipogenic genes. These results implicate miR-122 as a key regulator of cholesterol and fatty-acid metabolism in the adult liver and suggest that miR-122 may be an attractive therapeutic target for metabolic disease.
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Many miRNAs have evolved to regulate multiple components of certain pathways, thereby mediating more effective negative regulation on those pathways.
“This finding is in agreement with limited data from other laboratories that suggests that many miRNAs have evolved to regulate multiple components of certain pathways, thus mediating a more effective negative regulation on those pathways (33).”
From MicroRNA-21 Targets a Network of Key Tumor-Suppressive Pathways in Glioblastoma Cells (2008) · cites this paper as [33]
Inhibition of miR-122 reduces plasma cholesterol and hepatic steatosis, though the specific gene regulatory pathways involved are unclear.
“Inhibition of miR-122 reduces plasma cholesterol and hepatic steatosis, though the specific gene regulatory pathways involved are unclear.”
From The Vasculature in Prediabetes (2018) · cites this paper as [140]
The most abundant microRNA in the liver is miR-122.
“The most abundant microRNA in the liver is miR-122.”
From The Vasculature in Prediabetes (2018) · cites this paper as [140]
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- Authors
- Esau, C., Davis, S., Murray, S. F., Yu, X. X., Pandey, S. K., Pear, M., Watts, L., Booten, S. L., Graham, M., McKay, R., Subramaniam, A., Propp, S., Lollo, B. A., Freier, S., Bennett, C. F., Bhanot, S., & Monia, B. P.
- Affiliations
- Ionis Pharmaceuticals (United States) (US)
- Corresponding author
- Esau, Christine
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2006-02
- Volume
- 3
- Issue
- 2
- Pages
- 87-98
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2139342290
- Cited by
- 2,082
- References
- 43
- Citations by year
- 2026: 41 · 2025: 41 · 2024: 46 · 2023: 71 · 2022: 96 · 2021: 89 · 2020: 98 · 2019: 105 · 2018: 121 · 2017: 119 · 2016: 155 · 2015: 141 · 2014: 159 · 2013: 178 · 2012: 149
- FWCI
- 29.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of California, San Diego
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- miR-122, microRNA regulation, lipid metabolism, serum cholesterol, hepatic fatty acid oxidation, cholesterol biosynthesis, fatty acid synthesis, AMPK, diet-induced obesity, hepatic steatosis, lipogenic genes, therapeutic target
- MeSH terms
- Animals, Blood Chemical Analysis, Cell Line, Cholesterol, Chromatography, High Pressure Liquid, Enzyme Activation, Fatty Acids, Gene Expression Regulation, Liver, Molecular Sequence Data, Multienzyme Complexes, Obesity, Blotting, Northern, Blotting, Western, Oligonucleotides, Antisense, Protein Serine-Threonine Kinases, DNA Primers, Reverse Transcriptase Polymerase Chain Reaction, MicroRNAs, Microarray Analysis, Lipid Metabolism, Mice, AMP-Activated Protein Kinases
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