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10.1038/ncomms6215 http://scihub22266oqcxt.onion/10.1038/ncomms6215 C4205484!4205484!25333900     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2014 ; 5 (ä): ä Nephropedia Template TP {{tp|p=25333900|t=2014. Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts |pdf=|usr=}}{{25333900}} gab.com Text Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25333900 #FOAvip 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 signalling 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 nonselective S1P receptor agonist FTY720 causes increased bone formation in wild-type, 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. Twit Text FOAVip Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25333900 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25333900 #FOAvip English Wikipedia <ref>{{Cite pmid|25333900}}</ref> Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts #MMPMID25333900 Keller J; Catala-Lehnen P; Huebner AK; Jeschke A; Heckt T; Lueth A; Krause M; Koehne T; Albers J; Schulze J; Schilling S; Haberland M; Denninger H; Neven M; Hermans-Borgmeyer I; Streichert T; Breer S; Barvencik F; Levkau B; Rathkolb B; Wolf E; Calzada-Wack J; Neff F; Gailus-Durner V; Fuchs H; de Angelis MH; Klutmann S; Tsourdi E; Hofbauer LC; Kleuser B; Chun J; Schinke T; Amling M Nat Commun 2014[]; 5 (ä): ä PMID25333900show ga 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 signalling 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 nonselective S1P receptor agonist FTY720 causes increased bone formation in wild-type, 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. äCalcitonin controls bone formation by inhibiting the release of sphing(epmc).pdf DeepDyve Pubget Overpricing