{"owner": "ArrayExpress Uploader", "ownerprofile_id": "arrayexpress_sid", "species": "mouse", "factors": [{"GSM693652": {"GENOTYPE": "apoE-deficient", "ORGANISM PART": "failing heart", "TREATMENT": "2 months of rosiglitazone"}}, {"GSM693652": {"GENOTYPE": "apoE-deficient", "ORGANISM PART": "failing heart", "TREATMENT": "2 months of rosiglitazone"}}, {"GSM693654": {"GENOTYPE": "apoE-deficient", "ORGANISM PART": "heart", "TREATMENT": "none"}}, {"GSM693654": {"GENOTYPE": "apoE-deficient", "ORGANISM PART": "heart", "TREATMENT": "none"}}, {"GSM693656": {"GENOTYPE": "wild type", "ORGANISM PART": "control heart", "TREATMENT": "none"}}, {"GSM693656": {"GENOTYPE": "wild type", "ORGANISM PART": "control heart", "TREATMENT": "none"}}], "id": 6414, "pop_total": 0, "platform": 6, "summary_wrapped": "The anti-diabetic drug and agonist of the peroxisome proliferator-activated receptor gamma (Pparg), rosiglitazone, was recently withdrawn...", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 3, "sample_count": 6, "tags": ["atherosclerosis", "disease", "heart", "insulin", "lipid", "peroxisome"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_id_plat": "E-GEOD-28031_A-AFFY-45", "slug": "microarray-gene-expression-profiling-of-heart-fail", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-28031", "geo_gds_id": "", "name": "Microarray gene expression profiling of heart failure induced in apolipoprotein E-deficient mice by treatment with rosiglitazone", "created": "Nov.11, 2014", "summary": "The anti-diabetic drug and agonist of the peroxisome proliferator-activated receptor gamma (Pparg), rosiglitazone, was recently withdrawn in many countries because the drug use was associated with an increased risk of heart failure. To investigate underlying pathomechanisms, we chose 6-month-old apolipoprotein E (apoE)-deficient mice, which are prone to atherosclerosis and insulin resistance, and thereby mimic the risk profile of patients with cardiovascular disease. After 8 weeks of rosiglitazone treatment (30 mg/kg/day), echocardiography and histology analyses demonstrated that rosiglitazone had induced heart failure with cardiac dilation. Concomitantly, cardiac lipid overload and lipid-induced cardiomyocyte death developed. The microarray gene expression study of heart tissue from rosiglitazone-treated apoE-deficient mice relative to untreated apoE-deficient mice and non-transgenic B6 mice identified cardiac Pparg-dependent lipid metabolism genes in rosiglitazone-treated mice, which seem to trigger a major heart failure promoting pathway. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) rosiglitazone-treated 8-month-old apolipoprotein (apoE)-deficient mice with symptoms of heart failure, (ii) untreated 8-month-old apoE-deficient mice, and (iii) age-matched, untreated, non-transgenic B6 control mice.", "geo_gse_id": "E-GEOD-28031", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-28031/samples/"}