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Cell Type-specific Gene Expression Profiling in the Mouse Liver
Published on: September 17, 2019
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Integrated multiomics analysis reveals changes in liver physiological function in Aqp9 gene knockout mice.
Quancheng Cheng1, Junwei Zhang2, Huiru Ding1
1Department of Human Anatomy and Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
International Journal of Biological Macromolecules
|June 23, 2023
Summary
Removing Aquaporin 9 (AQP9) affects glycerol metabolism, causing liver damage and inflammation in mice. This highlights AQP9's crucial role in maintaining liver health and physiological balance.
Area of Science:
- Hepatology
- Molecular Biology
- Physiology
Background:
- Aquaporin 9 (AQP9) facilitates glycerol transport into hepatocytes, impacting liver osmotic regulation and energy metabolism.
- Previous research links AQP9 dysfunction to liver disease pathogenesis.
Purpose of the Study:
- To investigate the physiological role of AQP9 in the liver using a knockout mouse model.
- To elucidate the molecular consequences of AQP9 absence in liver tissue.
Main Methods:
- Generation of Aqp9 knockout (Aqp9-/-) mice.
- Comprehensive multi-omics analysis including transcriptomics, proteomics, and metabolomics.
Main Results:
- Aqp9 knockout mice exhibited reduced body weight due to altered glycerol metabolism.
- Loss of AQP9 led to hepatocyte death, inflammatory cell infiltration, and immune responses.
- Evidence of scattered, mild liver cell pyroptosis and compensatory proliferation was observed.
Conclusions:
- AQP9 is essential for maintaining liver physiological homeostasis.
- Aqp9 deficiency disrupts glycerol metabolism, triggers inflammation, and impacts liver cell viability and regeneration.

