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Gene expression in liver from WT/ACOX1 liver specific knockout mice

ABSTRACT: The target of this project is to investigate the effect of ACOX1 knockout in liver Gene expression profiling analysis were performed using data obtained from RNA-seq of two genotypes mice liver

ORGANISM(S): Mus musculus

PROVIDER: GSE227896 | GEO | 2024/03/20

REPOSITORIES: GEO

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Gene expression in liver from WT/ACOX1 liver specific knockout mice

Project description:Gene expression in liver from WT/ACOX1 liver specific knockout mice

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Effect of knockdown ACOX1 on gene expression in HK-2 cells

Project description:To investigate the role of ACOX1, we knocked down ACOX1 by shRNA in HK-2 cell lines and detected differential genes. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.

2024-02-02 | GSE205057 | GEO

Identifying the role of Acox1 in metabolism and inflammation in non-alcoholic fatty liver disease through mRNA-sequencing.

Project description:Purpose: To identify the impact of Acox1 on cellular metabolism and inflammation related to non-alcoholic fatty liver disease, within the context of obesogenic dietary stress. Methods: Hepatic mRNA profiles were obtained in triplicate for control and Acox1Lampe1 mice on chow diet or obesogenic diet. Profiles were generated using the Illumina HiSeq2000, reads that passed quality inspection were processed through the TopHap/Cufflinks pipeline. Results: Approximately 20million reads per sample were aligned to the mm8 mouse genome, using annotations provided by Ensembl. Testing between control and Acox1Lampe1 mice on control and obesogenic diets was performed using a 2-way ANOVA, with a p-value cutoff of 0.05 and FC of 1.5. We observed a significant alteration of hepatic gene expression in Acox1Lampe1 mutant mice, a pattern that was exacerbated by the obesogenic diet. Among significant genes, we observed an enrichment of those known to teb associated with inflammatory responses, leukocyte activation and adhesion, and abnormal liver physiology, regeneration, and development. Conclusion: Through next generation sequencing of hepatic tissues from control and Acox1Lampe1 mutant mice on control and obesogenic diets, we demonstrate that Acox1 regulates both metabolism and inflammation, the interplay of which correlates with increased hepatocellular damage and impared hepatic mitochondrial function.

2018-05-09 | GSE89626 | GEO

Proteomic analysis of liver from control and acox1 ko mice

Project description:Compare the proteome of control and Acox1 KO liver from mice

2022-10-26 | PXD037727 |

Label-free LC-MSMS proteomics for P30 Acox1 WT vs KO

Project description:Background: Dyslipidemia is a significant contributor to many eye diseases and the lipid processing pathways are not well understood. Peroxisomes oxidize very long-chain, monocarboxylic and dicarboxylic fatty acids. Genetic mutations in peroxisomal proteins may lead to severe neural retinal degeneration. However, there are limited approaches available for peroxisomal disease treatment. Method: In mice with genetic deficiency of ACOX1 (acyl-coenzyme A oxidase 1, the first and key metabolic enzyme in peroxisomal fatty acid oxidation), we characterized the retinal phenotype during development. Retinal function, thickness and photoreceptor structure were examined. Proteomics was utilized for molecular mechanistic investigation. Metabolomics and fatty acid profiling and were conducted to study the metabolic alterations in the retinas. Nutrient intervention was also applied to test if supplementation of lacking nutrients attenuated retinal dysfunction. Results: In one-month-old mice with ACOX1 deficiency, we found reduced neural retinal signaling, accompanied with decrease expression of genes involved in phototransduction. Proteomics identified decreased glucose and mitochondrial metabolism, supported by decreased mitochondrial DNA copy number. Metabolomics showed decreased retinal pyruvate and pyruvate supplementation from one-month old attenuated neural retinal dysfunction in ACOX1-deficient mice at 2 months. Furthermore, there was also a significant decrease in omega-3 fatty acids and a compensatory increase in omega-6 fatty acids. Dietary supplementation of docosahexaenoic acid (omega-3) or docosahexaenoic acid plus arachidonic acid (omega-6) improved neural retinal function in ACOX1-deficient mice. Conclusion: Retinal metabolic imbalance was observed in mice with peroxisomal fatty acid dysfunction. Nutrient intervention is an effective approach to attenuate the disease progression.

2025-12-15 | PXD055240 | Pride

Proteomics analysis for liver from WT and Hsd17b6 liver specific knockout mice

Project description:Eight weeks old LSL-Cas9 mice were injected with AAV2/8 expressing Cre driving by TBG promoter and sgRNA of gene of interest to specifically knockout gene in liver. In the present study, either control or sgHsd17b6 virus are injected. The mice are subjected to high fat choline dificient diet feeding for 8 weeks and then the liver samples were collected and subjected to Astral-DIA based proteomics analysis.

2024-10-02 | PXD056581 |

Transcription profiling of mouse adult male wild-type liver (M-WT), adult female wild-type liver (F-WT), adult male liver-specific HNF4alpha knockout liver (M-KO) and adult female liver-specific HNF4alpha knockout liver (F-KO) to investigate sex-dependent and HNF4alpha-dependent gene expression

Project description:A series of dual-channel gene expression profiles obtained using Rosetta/Agilent Whole Mouse Genome oligonucleotide microarrays, 4 x 44K format, was used to identify sex-dependent and HNF4alpha-dependent differences in gene expression in adult mouse liver. This series is comprised of four sex-genotype combinations: adult male wild-type liver (M-WT), adult female wild-type liver (F-WT), adult male liver-specific HNF4alpha knockout liver (M-KO) and adult female liver-specific HNF4alpha knockout liver (F-KO). Four pools, each comprised of 4 randomly selected individual liver RNAs, were prepared for each sex-genotype combination. The pools were paired randomly to generate 4 separate experimental comparisons: M-WT:F-WT (first array comparison), M-WT:M-KO (second array comparison), F-WT:F-KO (third array comparison), and M-KO:F-KO (fourth array comparison). A total of 4994 HNF4alpha-dependent genes were identified, of which ~1000 fewer genes responded to the loss of HNF4alpha in female liver as compared to male liver. Moreover, 90% of the genes showing sex-specific expression in the liver were shown to lose sex specificity in HNF4alpha-deficient liver. Experiment Overall Design: An Alexa555-labeled cDNA sample is co-hybridized with an Alexa647-labeled cDNA sample. The samples are then dye-swapped and compared again on a second microarray chip. Together, these two mixed cDNA samples are considered a fluorescent reverse pair (dye swap). Similarly, a second fluorescent reverse pair is generated and the two pairs are averaged. The normalized expression ratio for each array is reported along with the two separate intensities. In this way, dye swaps were carried out for each of the four experimental comparisons. Thus, four microarrays, one for each mixed cDNA sample, were hybridized for each of the four fluorescent reverse pairs, giving a total of 16 microarrays.

2008-04-04 | E-GEOD-10390 | biostudies-arrayexpress

Ube4a liver-specific knockout effect on fasted liver

Project description:Ube4a liver-specific knockout effect on fasted liver

| PRJNA1109779 | ENA

Transcription profiling of liver-specific Hnf4alpha knockout and wild type mouse liver

Project description:Gene expression differences between wild-type and liver-specific Hnf4alpha knockout (Albumin Cre+/-; Hnf4 fl/fl) mouse liver were assessed using RNA obtained from 2-month-old control and genetically modified female mice. RNA was hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 arrays [Mouse430_2].

2009-04-01 | E-MEXP-1733 | biostudies-arrayexpress

Hepatocyte RNA-seq analysis in liver-specific XBP1 knockout mice fed a high fat sugar diet

Project description:X-box binding protein 1 (XBP1) is a key component of the unfolded protein response (UPR) and plays important roles in the pathogenesis of nonalcoholic fatty liver diseases (NAFLD). Mice with liver-specific XBP1 deletion developed great liver injury and fibrosis in a dietary model of NAFLD. This project is to investigate hepatocyte-specific transcriptome profiling in XBP1-deficient mice fed a high fat sugar diet.

2022-01-03 | GSE190947 | GEO

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