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| Status |
Public on Feb 15, 2018 |
| Title |
Hepatic loss of Lis1 leads to fatty liver and predisposes to tumorigenesis in mice |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
We found that genetic deletion of Lis1 (also known as Pafah1b1) in mouse liver led to increased lipid accumulation and inflammation in the liver. Further analysis revealed that loss of Lis1 led to endoplasmic reticulum (ER) stress and reduced triglyceride secretion. Attenuation of ER stress by tauroursodeoxycholic acid (TUDCA) diminished lipid accumulation in the Lis1 defecient hepatocytes. In addition, Golgi was disorganized in Lis1 deficient livers. These mutants exhibited increased hepatocyte ploidy and accelerated development of liver cancer when treated with DEN. Taken together, these findings suggest that Lis1 is involved in the development and progression of liver diseases from steatosis to liver cancer and provide a useful model for delineating the molecular pathways that lead to these diseases.
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| |
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| Overall design |
Gene expression in 4 control livers (CT) and 4 Lis1 knockout livers (KO) at 2 months was analyzed by RNA-Seq.
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| |
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| Contributor(s) |
Li X, Song H |
| Citation(s) |
29475944 |
| |
| Submission date |
Dec 14, 2017 |
| Last update date |
Mar 21, 2019 |
| Contact name |
Xiaoling Li |
| E-mail(s) |
lxling@zju.edu.cn
|
| Phone |
+86-571-88208368
|
| Organization name |
Zhejiang University
|
| Department |
Life Sciences Institute
|
| Lab |
Hai Song Lab
|
| Street address |
866
|
| City |
hangzhou |
| State/province |
Zhejiang |
| ZIP/Postal code |
310058 |
| Country |
China |
| |
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| Platforms (1) |
| GPL17021 |
Illumina HiSeq 2500 (Mus musculus) |
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| Samples (8)
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| Relations |
| BioProject |
PRJNA422444 |
| SRA |
SRP126777 |
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