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Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts

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Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts. / Keller, Johannes; Catala-Lehnen, Philip; Hübner, Antje K.; Jeschke, Anke; Heckt, Timo; Lueth, Anja; Krause, Matthias; Koehne, Till; Albers, Joachim; Schulze, Jochen; Schilling, Sarah; Haberland, M; Denninger, Hannah; Neven, Mona; Hermans-Borgmeyer, Irm; Streichert, Thomas; Breer, Stefan; Barvencik, Florian; Levkau, Bodo; Rathkolb, Birgit; Wolf, Eckhard; Calzada-Wack, Julia; Neff, Frauke; Gailus-Durner, Valerie; Fuchs, Helmut; de Angelis, Martin Hrabĕ; Klutmann, Susanne; Tsourdi, Elena; Hofbauer, Lorenz C; Kleuser, Burkhard; Chun, Jerold; Schinke, Thorsten; Amling, Michael.

In: NAT COMMUN, Vol. 5, 2014, p. 5215.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Keller, J, Catala-Lehnen, P, Hübner, 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 2014, 'Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts', NAT COMMUN, vol. 5, pp. 5215. https://doi.org/10.1038/ncomms6215

APA

Keller, J., Catala-Lehnen, P., Hübner, A. K., 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., ... Amling, M. (2014). Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts. NAT COMMUN, 5, 5215. https://doi.org/10.1038/ncomms6215

Vancouver

Keller J, Catala-Lehnen P, Hübner AK, Jeschke A, Heckt T, Lueth A et al. Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts. NAT COMMUN. 2014;5:5215. https://doi.org/10.1038/ncomms6215

Bibtex

@article{2f8a54ac4e2e4f12ba99b918cfe702cf,
title = "Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts",
abstract = "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.",
author = "Johannes Keller and Philip Catala-Lehnen and H{\"u}bner, {Antje K.} and Anke Jeschke and Timo Heckt and Anja Lueth and Matthias Krause and Till Koehne and Joachim Albers and Jochen Schulze and Sarah Schilling and M Haberland and Hannah Denninger and Mona Neven and Irm Hermans-Borgmeyer and Thomas Streichert and Stefan Breer and Florian Barvencik and Bodo Levkau and Birgit Rathkolb and Eckhard Wolf and Julia Calzada-Wack and Frauke Neff and Valerie Gailus-Durner and Helmut Fuchs and {de Angelis}, {Martin Hrabĕ} and Susanne Klutmann and Elena Tsourdi and Hofbauer, {Lorenz C} and Burkhard Kleuser and Jerold Chun and Thorsten Schinke and Michael Amling",
year = "2014",
doi = "10.1038/ncomms6215",
language = "English",
volume = "5",
pages = "5215",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts

AU - Keller, Johannes

AU - Catala-Lehnen, Philip

AU - Hübner, Antje K.

AU - Jeschke, Anke

AU - Heckt, Timo

AU - Lueth, Anja

AU - Krause, Matthias

AU - Koehne, Till

AU - Albers, Joachim

AU - Schulze, Jochen

AU - Schilling, Sarah

AU - Haberland, M

AU - Denninger, Hannah

AU - Neven, Mona

AU - Hermans-Borgmeyer, Irm

AU - Streichert, Thomas

AU - Breer, Stefan

AU - Barvencik, Florian

AU - Levkau, Bodo

AU - Rathkolb, Birgit

AU - Wolf, Eckhard

AU - Calzada-Wack, Julia

AU - Neff, Frauke

AU - Gailus-Durner, Valerie

AU - Fuchs, Helmut

AU - de Angelis, Martin Hrabĕ

AU - Klutmann, Susanne

AU - Tsourdi, Elena

AU - Hofbauer, Lorenz C

AU - Kleuser, Burkhard

AU - Chun, Jerold

AU - Schinke, Thorsten

AU - Amling, Michael

PY - 2014

Y1 - 2014

N2 - 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.

AB - 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.

U2 - 10.1038/ncomms6215

DO - 10.1038/ncomms6215

M3 - SCORING: Journal article

C2 - 25333900

VL - 5

SP - 5215

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -