Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse poloxamer P-407 chronic hyperlipidemia mouse model

ABSTRACT: We performed a systemic study of the poloxamer P-407-induced chronic hyperlipidemia in C57BL/6J mice. Mice were treated 96 days every third day.The poloxamer mostly elevates plasma triglycerides and cholesterol while change of the liver cholesterol is not significant. Experiment Overall Design: A group of 12 mice were administered 0.5 g/kg poloxamer P-407 by intraperitoneal (i.p.) injection (poloxamere group), a control group of 4 mice were injected every third day with normal saline. Total RNA from P-407 treated 12 mice has been pooled into 3 biological replicas (Smpl1, Smpl2 and Smpl3). Reference total RNA has been obtained by pooling 4 mice from control group. Each RNA sample has been splitted and hybridised in parallel on cDNA (G4104A) and oligonucleotide (G4120A) mouse microarrays (Agilent Technologies, CA, USA.

ORGANISM(S): Mus musculus

SUBMITTER: Drago Kuzman

PROVIDER: E-GEOD-6305 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:C57BL/6 mice were fed ad libitum for the first 5 days of the experiments with high fat high cholesterol (HFC) diet only. The next 7 days of the experiments mice were continuously fed on a HFC diet and simultaneously vehicle (control group), fenofibrate (100 mg/kg) or lovastatin (30 mg/kg) were orally daily administered. At the end of the experiment (day 12) fenofibrate and lovastatin significantly decreased plasma LDL levels, while plasma cholesterol levels were significantly decreased by lovastatin only. Gene expression analysis of hyperlipidemic mouse liver revealed 391 significantly modulated genes when compared to standard diet fed mice. KEGG pathways related to modulated genes were identified and the most significant were biosynthesis of steroids, metabolism of xenobiotics by cytochrome P450 and linoleic acid metabolism. These pathways were modulated in a way, which increased the clearance of lipids and decreased endogenous synthesis of fatty acids and cholesterol. Additionally, genes involved in the regulation of detoxification pathways were significantly upregulated. The hepatic gene expression profiles of fenofibrate and lovastatin-treated HFC diet fed mice were compared to the vehicle-treated HFC diet fed mice. In the fenofibrate-treated group 124 genes and in the lovastatin-treated group 38 genes were significantly modulated. In the fenofibrate-treated group the top three significantly modulated pathways are fatty acid metabolism, propanoate metabolism and ascorbate and aldarate metabolism. While in the lovastatin-treated group the top three significantly modulated pathways are glycosphingolipid biosynthesis, tyrosine metabolism and metabolism of xenobiotics by cytochrome P450. Expert based classification revealed that both fenofibrate an lovastatin significantly down-regulated genes encoding sterol-C4-methyl oxidase like and 7-dehydrocholesterol reductase. Additionally, the regulation of cholesterol at the transcriptional level was also significantly augmented by fenofibrate and lovastatin, as judged by increased expression of -1 and decreased expression of INSIG-2. Experiment Overall Design: 24 seven week old mice were randomly divided in four experimental groups. Control group (n = 6) was fed on a standard chow diet (diet 3430, Provimi Kliba AG, Kaiseraugst, Switzerland) and treated orally once daily with vehicle for 12 days. Remaining 18 mice were fed on HFC diet for 12 days. On day five HFC diet fed mice were treated orally once daily either with vehicle (HFC group, n=6), lovastatin (HFC lovastatin group, 30mg/kg, n=6) or fenofibrate (HFC fenofibrate group, 100mg/kg, n=6). Doses of lovastatin and fenofibrate were choosen according to the literature review. On day 12 liver were excised and immediately frozen in liquid nitrogen and stored at -80Â°C for the subsequent transriptome analyses

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Transcription profiling of mouse poloxamer P-407 chronic hyperlipidemia mouse model

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