{"owner": "ArrayExpress Uploader", "pop_total": 0, "id": 6624, "factors": [{"GSM794238": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "control"}}, {"GSM794238": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "control"}}, {"GSM794238": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "control"}}, {"GSM794238": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "control"}}, {"GSM794242": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "control"}}, {"GSM794242": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "control"}}, {"GSM794242": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "control"}}, {"GSM794242": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "control"}}, {"GSM794246": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "Rosiglitazone (Rosi)"}}, {"GSM794246": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "Rosiglitazone (Rosi)"}}, {"GSM794246": {"MONOCYTE SUBTYPE": "Ly6Chi", "TREATMENT": "Rosiglitazone (Rosi)"}}, {"GSM794249": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "Rosiglitazone (Rosi)"}}, {"GSM794249": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "Rosiglitazone (Rosi)"}}, {"GSM794249": {"MONOCYTE SUBTYPE": "Ly6Clo", "TREATMENT": "Rosiglitazone (Rosi)"}}], "ownerprofile_id": "arrayexpress_sid", "platform": 6, "summary_wrapped": "PPAR\u03b3 is known for its anti-inflammatory actions in macrophages. However, which macrophage populations express PPAR\u03b3 in vivo and how it...", "pubmed_id": 22855714, "geo_gse_id": "E-GEOD-32034", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 2, "sample_count": 14, "tags": ["leukocyte", "lipid", "lung", "macrophage", "monocyte", "pulmonary alveolar proteinosis", "spleen"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "tissue-specific-differences-in-ppar-control-of-mac", "geo_id_plat": "E-GEOD-32034_A-AFFY-45", "name": "Tissue-specific differences in PPAR\u03b3 control of macrophage function.", "created": "Nov.11, 2014", "summary": "PPAR\u03b3 is known for its anti-inflammatory actions in macrophages. However, which macrophage populations express PPAR\u03b3 in vivo and how it regulates tissue homeostasis in the steady state and during inflammation is not completely understood. We show that lung and spleen macrophages constitutively expressed PPAR\u03b3, while other macrophage populations did not. Recruitment of monocytes to sites of inflammation was associated with induction of PPAR\u03b3 as they differentiated to macrophages. Its absence in these macrophages led to failed resolution of inflammation, characterized by persistent, low-level recruitment of leukocytes. Conversely, PPAR\u03b3 agonists supported an earlier cessation in leukocyte recruitment during resolution of acute inflammation and likewise suppressed monocyte recruitment to chronically inflamed atherosclerotic vessels. In the steady state, PPAR\u03b3 deficiency in macrophages had no obvious impact in the spleen but profoundly altered cellular lipid homeostasis in lung macrophages. Reminiscent of pulmonary alveolar proteinosis, LysM-Cre x PPAR\u03b3flox/flox mice displayed mild leukocytic inflammation in the steady-state lung and succumbed faster to mortality upon infection with S. pneumoniae. Surprisingly, this mortality was not due to overly exuberant inflammation, but instead to impaired bacterial clearance. Thus, in addition to its anti-inflammatory role in promoting resolution of inflammation, PPAR\u03b3 sustains functionality in lung macrophages and thereby has a pivotal role in supporting pulmonary host defense. The two major subsets of monocytes (Ly-6C+ and Ly-6Clo) from 12-week old C57Bl/6 mice were sorted and the RNA extracted and hybridized to Affymetrix GeneChip\u00ae 430 2.0 arrays. We pooled leukocytes from 5 mice for each sort and sorted 3 to 4 separate times for 3 to 4 biological replicates.", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-32034", "species": "mouse", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-32034/samples/"}