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Transcription profiling of mouse 3T3-L1 adipocyte tissue culture treated with tunicamycin

ABSTRACT: Tunycamcin induces UPR/ISR and Inflammation in mouse 3T3-L1 adipocyte tissue culture. The early transcriptome changes were analyzed using high-density microarrays to better characterize the signaling pathways responding to tunicamycin, to be compared with similar experiments with CLA as the treatment. Their gene expression responses between 4 to 12 hr after treatment showed a common set of early gene expression changes indicative of a UPR/Inflammation stress response. Experiment Overall Design: Mouse 3T3-L1 RNA for each time point was isolated from control and treatment samples for analysis on microarrays with two biological reps.

ORGANISM(S): Mus musculus

SUBMITTER: Jean-Jack Riethoven

PROVIDER: E-GEOD-8682 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Trans-10, cis-12 conjugated linoleic acid activates the integrated stress response pathway in adipocytes.

LaRosa P Christopher PC Riethoven Jean-Jack M JJ Chen Han H Xia Yuannan Y Zhou You Y Chen Mei M Miner Jess J Fromm Michael E ME

Physiological genomics 20070918 3

Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) causes fat loss in mouse white adipose tissue (WAT) and adipocytes in culture. The early transcriptome changes in treated WAT and 3T3-L1 adipocytes were analyzed using high-density microarrays to better characterize the signaling pathways responding to t10c12 CLA. Gene expression responses between 4 and 24 h after treatment showed a common set of early gene expression changes indicative of an integrated stress response (ISR). The responses o ...[more]

PMID: 17878318

Similar Datasets

Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with tunicamycin

Project description:Tunycamcin induces UPR/ISR and Inflammation in mouse 3T3-L1 adipocyte tissue culture. The early transcriptome changes were analyzed using high-density microarrays to better characterize the signaling pathways responding to tunicamycin, to be compared with similar experiments with CLA as the treatment. Their gene expression responses between 4 to 12 hr after treatment showed a common set of early gene expression changes indicative of a UPR/Inflammation stress response. Keywords: control/treatment time course

2008-01-11 | GSE8682 | GEO

Transcription profiling of mouse 3T3-L1 adipocyte tissue culture treated with CLA

Project description:Trans-10, Cis-12 conjugated linoleic acid (t10c12 CLA) causes fat loss in mouse 3T3-L1 adipocyte tissue culture. The early transcriptome changes were analyzed using high-density microarrays to better characterize the signaling pathways responding to t10c12 CLA. Their gene expression responses between 4 to 24 hr after treatment showed a common set of early gene expression changes indicative of an integrated stress response (ISR). Experiment Overall Design: Mouse 3T3-L1 RNA for each time point was isolated from control and treatment samples for analysis on microarrays with two to four biological reps.

2008-06-16 | E-GEOD-8681 | biostudies-arrayexpress

Transcription profiling of mouse 3T3-L1 adipocyte tissue culture treated with cis-9,trans-11 conjugated linoleic acid(c9t11 CLA)

Project description:Trans-10, Cis-12 conjugated linoleic acid (t10c12 CLA) causes fat loss in mouse 3T3-L1 adipocyte tissue culture; however cis-9, trans-11 CLA does not (this series). The early transcriptome changes were analyzed using high-density microarrays to better characterize the signaling pathways responding to c9t11 CLA. Their gene expression responses between 8 to 12 hr after treatment showed no gene expression changes indicative of an integrated stress response (ISR). Experiment Overall Design: Mouse 3T3-L1 RNA for each time point was isolated from control and treatment samples for analysis on microarrays; there are four biological reps for the controls for each timepoint, and only one rep for the treatment.

2008-06-16 | E-GEOD-8684 | biostudies-arrayexpress

Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with CLA

2008-01-11 | GSE8681 | GEO

Transcription profiling of mouse 3T3-L1 tissue (preadipocytes) treated with trans-10,Cis-12 conjugated linoleic acid(t10c12 CLA)

Project description:Trans-10, Cis-12 conjugated linoleic acid (t10c12 CLA) causes fat loss in mouse white adipose tissue (WAT) and 3T3-L1 adipocyte tissue culture; however in preadipocyte tissue (this series) the UPS/ISR and fat loss is not detected. The early transcriptome changes in 3T3-L1 preadipocyte tissue culture were analyzed using high-density microarrays to better characterize the signaling pathways responding to t10c12 CLA. Their gene expression responses between 4 to 12 hr after treatment do not show a set of genes indicative of an integrated stress response (ISR). Experiment Overall Design: Mouse 3T3-L1 RNA for each time point was isolated from two control (LA) and two treatment (CLA) samples for analysis on four microarrays.

2008-06-16 | E-GEOD-8683 | biostudies-arrayexpress

Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with cis-9,trans-11 conjugated linoleic acid(c9t11 CLA)

2008-01-11 | GSE8684 | GEO

Gene expression in 3T3-L1 mouse tissue (preadipocytes) treated with Trans-10,Cis-12 conjugated linoleic acid(t10c12 CLA)

2008-01-11 | GSE8683 | GEO

Conjugated linoleic acid activates AMPK and reduces adiposity more effectively when used with metformin

Project description:Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) causes dramatic reductions in white adipose tissue in mice but has had limited effectiveness in humans. Determination of the signaling pathways involved may lead to better regulation of adiposity. T10c12 CLA was found to activate AMP-activating protein kinase (AMPK), a central regulator of cell metabolism. Compound C, a potent inhibitor of AMPK, prevents many of the typical responses to treatments with t10c12 CLA including the integrated stress response (ISR), the inflammatory response, the reduction in key lipogenic transcription factors, and delipidation. Treatment of adipocytes or mice with t10c12 CLA in conjunction with AMPK activator metformin results in more delipidation than treatment with the individual chemicals. Additionally, the combination showed a reduced inflammatory response relative to a t10c12 CLA treatment alone. The combination of t10c12 CLA and metformin, widely used to treat insulin resistance and Type II diabetes, has potential as a treatment for reducing adiposity in humans. Keywords: control/treatment Mouse 3T3-L1 RNA for was isolated from control linoleic acid (LA) and treatment (CLA, CLA+metformin, metformin) samples for analysis on microarrays with three biological reps.

2009-11-01 | E-GEOD-14888 | biostudies-arrayexpress

Transcription profiling of mouse adipocytes treated with trans-10, cis-12 conjugated linoleic acid activates the integrated stress response pathway in adipocytes (GEO Super Series)

Project description:This SuperSeries is composed of the following subset Series:; GSE8679: Gene expression in mouse white adipose tissue; GSE8681: Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with CLA; GSE8682: Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with tunicamycin; GSE8683: Gene expression in 3T3-L1 mouse tissue (preadipocytes) treated with Trans-10,Cis-12 conjugated linoleic acid(t10c12 CLA); GSE8684: Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with cis-9,trans-11 conjugated linoleic acid(c9t11 CLA) Experiment Overall Design: Refer to individual Series

2008-06-20 | E-GEOD-11384 | biostudies-arrayexpress

Activated AMPK and prostaglandins are involved in the response to conjugated linoleic acid and are sufficient to cause lipid reductions in adipocytes

Project description:Activated AMPK and prostaglandins are involved in the response to conjugated linoleic acid and are sufficient to cause lipid reductions in adipocytes. Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) reduces triglyceride levels in adipocytes. AMP-activated protein kinase (AMPK) was recently demonstrated to be involved in the emerging pathways regulating this response. This study investigated the role of AMPK and inflammation in lowering triglyceride levels by testing the following hypotheses: 1) A moderate activator of AMPK, such as metformin, and an inflammatory response are sufficient to reduce triglycerides, and 2) Strong activation of AMPK is also sufficient. These experiments were performed by adding compounds that affect these pathways and measuring their effects in 3T3-L1 adipocytes. Tumor necrosis factor α (TNF-α), an inflammatory cytokine, increased the ability of metformin to reduce triglycerides, but TNF-α was observed to activate AMPK. A comparison of metformin, phenformin, TNF-α, and t10c12 CLA found a correlation between AMPK activity level and triglyceride reduction. Inhibitors of the prostaglandin (PG) biosynthetic pathway interfered with t10c12 CLA's ability to reduce triglycerides. Inhibitors of MAPK/ERK kinase or Jun N-terminal kinase interfered with the phosphorylation of phospholipase A2 and triglyceride reductions. Keywords: control/treatment Mouse 3T3-L1 RNA was isolated from control (LA) and treatment (CLA, phenformin) samples for analysis on microarrays with three biological replicates per sample. Limma data are available in the Supplementary files 'GSE17404_limma_CLAvsLA.txt', 'GSE17404_limma_PFMvsLA.txt', and 'GSE17404_limma_PFMvsCLA.txt'.

2010-08-10 | E-GEOD-17404 | biostudies-arrayexpress

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