{"owner": "ArrayExpress Uploader", "ownerprofile_id": "arrayexpress_sid", "species": "mouse", "factors": [{"GSM54999": {"GENOTYPE/VARIATION": "Col1-Dlk1"}}, {"GSM549992": {"GENOTYPE/VARIATION": "wild type"}}], "id": 8258, "pop_total": 0, "platform": 7, "summary_wrapped": "DLK1/FA-1 (delta-like 1/fetal antigen-1) is a transmembrane protein belonging to Notch/Delta family that acts as a membrane-associated or...", "geo_gse_id": "E-GEOD-22113", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 1, "sample_count": 2, "tags": ["body", "bone", "bone marrow", "estrogen", "membrane", "notch", "osteoblast", "protein", "volume"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_id_plat": "E-GEOD-22113_A-AFFY-23", "slug": "dlk1-is-a-novel-regulator-of-bone-mass-that-mediat", "geo_gds_id": "", "name": "DLK1 Is a Novel Regulator of Bone Mass That Mediates Estrogen-Deficiency Induced Bone Loss in Mice", "created": "Nov.23, 2014", "summary": "DLK1/FA-1 (delta-like 1/fetal antigen-1) is a transmembrane protein belonging to Notch/Delta family that acts as a membrane-associated or a soluble protein to regulate regeneration of a number of adult tissues. Here, we examined the role of DLK1/FA-1 in bone biology using osteoblast-specific-Dlk1 over-expressing mice (Col1-Dlk1). Col1-Dlk1 mice displayed growth retardation and significantly reduced total body weight and bone mineral density (BMD). \u03bcCT-scanning revealed a reduced trabecular and cortical bone volume fraction. Tissue-level histomorphometric analysis demonstrated decreased bone formation rate and enhanced bone resorption in Col1-Dlk1 as compared to WT. At a cellular level, DLK1 markedly reduced the total number of bone marrow (BM)-derived CFU-F, as well as their osteogenic capacity. In a number of in vitro culture systems, DLK1 stimulated osteoclastogenesis indirectly through osteoblast-dependent increased production of pro-inflammatory bone resorbing cytokines (e.g, Il7, Tnfa and Ccl3). We found that ovariectomy (ovx)-induced bone loss was associated with increased production of DLK1 in bone marrow by activated T-cells. However, Dlk1-/- mice were protected from ovx-induced bone loss. Thus, we identified DLK1 as a novel regulator of bone mass that function to inhibit bone formation and to stimulate bone resorption. Increasing DLK1 production by T-cells under estrogen deficiency suggests its possible use as a therapeutic target for preventing postmenopausal bone loss. Calvarial osteoblasts were grown from neonatal mice overexpressing Dlk1 and their non-transgenic littermate controls. Three separate cultures from each of the two genotypes were combined and analysed by Affymetrix microarray MOE430 2.0.", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22113", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22113/samples/"}