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GEO help: Mouse over screen elements for information. |
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| Status |
Public on Jan 16, 2017 |
| Title |
Gene expression profiles of livers from male LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed normal chow or high fat diet |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
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| Summary |
To investigate the molecular basis for male-specific steatohepatitis in Lamin A/C-deficient livers, microarray gene expression analysis was performed on total liver RNA isolated from 26- to 39-week-old, male LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed either normal chow (NC) or high fat diet plus carbohydrate-supplemented water (HFD).
Lamins are nuclear intermediate filament proteins that comprise the major components of the nuclear lamina in metazoan cells. Mutations in LMNA, which encodes lamins A/C, cause diseases termed laminopathies, including lipodystrophy, cardiomyopathy, and premature aging. The lamin A/C mutation-associated Dunnigan familial partial lipodystrophy is typically accompanied by fatty liver disease. The role of lamins in the liver is unknown, and it is unclear whether laminopathy-associated liver disease is due to primary hepatocyte defects or systemic alterations. To address these questions, mice carrying a hepatocyte-specific deletion of Lmna (KO mice) were generated. KO hepatocytes manifested abnormal nuclear morphology, and KO mice developed spontaneous male-selective hepatosteatosis, with increased susceptibility to high fat diet-induced steatohepatitis and fibrosis. The molecular mechanism by which liver-specific Lamin A/C deficiency induces male-specific steatohepatitis is unknown. The microarray data presented here demonstrates that hepatic Lmna deficiency is associated with upregulated expression of fatty acid transporters, lipid biosynthetic enzymes, lipid-droplet associated proteins, and interferon-regulated genes and other pro-inflammatory mediators.
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| Overall design |
Global gene expression profiling of liver RNA isolated from 26- to 39-week-old LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed either normal chow (NC) or high fat diet plus carbohydrate-supplemented water (HFD). The following mouse livers were used in gene expression profiling: LMNA+/+; Alb-Cre+, NC-fed (n=2); LMNA flx/+; Alb-Cre+, NC-fed (n=3); LMNA flx/flx; Alb-Cre+, NC-fed (n=3); LMNA flx/+; Alb-Cre+, HFD-fed (n=3); and LMNA flx/flx; Alb-Cre+, HFD-fed (n=3).
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| Contributor(s) |
Kwan R, Omary B |
| Citation(s) |
28913408 |
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| Submission date |
Jan 15, 2017 |
| Last update date |
Jan 18, 2023 |
| Contact name |
Raymond Kwan |
| E-mail(s) |
[email protected]
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| Phone |
7346476461
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| Organization name |
University of Michigan, Ann Arbor
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| Department |
Molecular and Integrative Physiology
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| Street address |
7720 Med Sci II
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| City |
Ann Arbor |
| State/province |
MI |
| ZIP/Postal code |
48109 |
| Country |
USA |
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| Platforms (1) |
| GPL17400 |
[MoGene-2_1-st] Affymetrix Mouse Gene 2.1 ST Array [transcript (gene) version] |
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| Samples (14)
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| Relations |
| BioProject |
PRJNA361410 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE93643_RAW.tar |
59.6 Mb |
(http)(custom) |
TAR (of CEL) |
| Processed data included within Sample table |
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