{"owner": "ArrayExpress Uploader", "pop_total": 0, "species": "mouse", "factors": [{"GSM1487524": {"treatment": "untreated", "genotype": "wildtype"}}, {"GSM1487524": {"treatment": "untreated", "genotype": "wildtype"}}, {"GSM1487524": {"treatment": "untreated", "genotype": "wildtype"}}, {"GSM1487527": {"treatment": "Calcitonin", "genotype": "wildtype"}}, {"GSM1487527": {"treatment": "Calcitonin", "genotype": "wildtype"}}, {"GSM1487527": {"treatment": "Calcitonin", "genotype": "wildtype"}}, {"GSM1487530": {"treatment": "untreated", "genotype": "Calcr-/-"}}, {"GSM1487530": {"treatment": "untreated", "genotype": "Calcr-/-"}}, {"GSM1487530": {"treatment": "untreated", "genotype": "Calcr-/-"}}, {"GSM1487533": {"treatment": "Calcitonin", "genotype": "Calcr-/-"}}, {"GSM1487533": {"treatment": "Calcitonin", "genotype": "Calcr-/-"}}, {"GSM1487533": {"treatment": "Calcitonin", "genotype": "Calcr-/-"}}], "id": 7695, "ownerprofile_id": "arrayexpress_sid", "platform": 6, "summary_wrapped": "The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice...", "geo_gse_id": "E-GEOD-60761", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 2, "sample_count": 12, "tags": ["bone", "calcitonin", "hormone", "lipid", "osteoclast"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "calcitonin-controls-bone-formation-by-inhibiting-t", "geo_id_plat": "E-GEOD-60761_A-AFFY-45", "name": "Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts", "created": "Nov.12, 2014", "summary": "The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the non-selective S1P receptor agonist FTY720 causes increased bone formation in wildtype, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo, and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts. Osteoclasts of wildtype and Calcr-/- C57Bl/6 mice were treated with Calcitonin and compared to the non-treated osteoclasts of wildtype or Calcr-/- mice, respectively.", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-60761", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-60761/samples/"}