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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)

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Jean-Jack Riethoven

PROVIDER: E-GEOD-11384 | 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

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

2008-01-11 | GSE8683 | 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

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

2008-01-11 | GSE8681 | GEO

Gene expression in 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). Keywords: control/treatment time course

2008-01-11 | GSE8684 | GEO

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

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

Microarray analysis reveals differential effects of conjugated linoleic acid isomers in ritonavir-treated 3T3-L1 adipocytes

Project description:Objective: To quantify changes in adipogenic gene expression in the presence of ritonavir (RTV) or tenofovir (TDF), and determine whether conjugated linoleic acid (CLA) isomers (cis9,trans11 or trans10,cis12) can mitigate detrimental effects of antiretoviral drugs. Methods: Affymetrix Mouse Genome 430 2.0 microarray was used to investigate gene expression in 3T3-L1 adipocytes treated with (1) RTV, TDF or ethanol control, or (2) ritonavir +c9,t11-CLA, ritonavir+t10,c12-CLA or ritonavir+DMSO control. RT-PCR validation of Pparg, Adipoq and Retn was carried out. ELISA and DNA binding ELISA were used to investigate secreted proteins and Pparg binding to its gene response element. Oil Red O staining was used to investigate triglyceride accumulation. Results: No effect was observed for TDF. Expression of 389 genes was altered more than 5-fold in the presence of RTV. Down-regulated genes included Pparg, Adipoq, Retn, Cfd and Cidec. Pparg and Adipoq down-regulation were confirmed by RT-PCR. PPAR-Î³ binding to its gene response element, adiponectin protein secretion and triglyceride accumulation were decreased by RTV. t10,c12-CLA in the presence of RTV decreased the expression of Ppargand Adipoq in microarray and RT-PCR. c9,t11-CLA increased PPAR-Î³ binding to its gene response element. Both isomers increased triglyceride storage in the presence of RTV. Conclusion: Ritonavir altered genes involved in adipocyte differentiation, lipid accumulation and glucose metabolism. Down-regulation of Pparg may be mediated by changes in Cepba and regulatory genes Pparg1c and Nr1h3. 3T3-L1 adipocytes were treated with ritonavir (20Î¼M; n=4), tenofovir (1Î¼M; n=4) or vehicle control (ethanol 0.1%; n=4) for 5 days and in a second experiment with ritonavir (20 ÂµM) +c9,t11-CLA (100Î¼M; n=4), ritonavir (20 ÂµM) +t10,c12-CLA (100Î¼M; n=4) or ritonavir+fatty acid vehicle control (DMSO 0.1%; n=4) for 5 days.

2016-07-07 | E-GEOD-70854 | 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

Mus musculus

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

| PRJNA109039 | ENA

Microarray analysis reveals differential effects of conjugated linoleic acid isomers in ritonavir-treated 3T3-L1 adipocytes

Project description:Objective: To quantify changes in adipogenic gene expression in the presence of ritonavir (RTV) or tenofovir (TDF), and determine whether conjugated linoleic acid (CLA) isomers (cis9,trans11 or trans10,cis12) can mitigate detrimental effects of antiretoviral drugs. Methods: Affymetrix Mouse Genome 430 2.0 microarray was used to investigate gene expression in 3T3-L1 adipocytes treated with (1) RTV, TDF or ethanol control, or (2) ritonavir +c9,t11-CLA, ritonavir+t10,c12-CLA or ritonavir+DMSO control. RT-PCR validation of Pparg, Adipoq and Retn was carried out. ELISA and DNA binding ELISA were used to investigate secreted proteins and Pparg binding to its gene response element. Oil Red O staining was used to investigate triglyceride accumulation. Results: No effect was observed for TDF. Expression of 389 genes was altered more than 5-fold in the presence of RTV. Down-regulated genes included Pparg, Adipoq, Retn, Cfd and Cidec. Pparg and Adipoq down-regulation were confirmed by RT-PCR. PPAR-γ binding to its gene response element, adiponectin protein secretion and triglyceride accumulation were decreased by RTV. t10,c12-CLA in the presence of RTV decreased the expression of Ppargand Adipoq in microarray and RT-PCR. c9,t11-CLA increased PPAR-γ binding to its gene response element. Both isomers increased triglyceride storage in the presence of RTV. Conclusion: Ritonavir altered genes involved in adipocyte differentiation, lipid accumulation and glucose metabolism. Down-regulation of Pparg may be mediated by changes in Cepba and regulatory genes Pparg1c and Nr1h3.

2016-07-07 | GSE70854 | GEO

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