Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis

Standard

Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis. / Liu, Peng; Lee, Sooyeon; Knoll, Jeanette; Rauch, Alexander; Ostermay, Susanne; Luther, Julia; Malkusch, Nicole; Lerner, Ulf H; Zaiss, Mario M; Neven, Mona; Wittig, Rainer; Rauner, Martina; David, Jean-Pierre; Bertolino, Philippe; Zhang, Chang X; Tuckermann, Jan P.

in: CELL DEATH DIFFER, Jahrgang 24, Nr. 4, 04.2017, S. 672-682.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Liu, P, Lee, S, Knoll, J, Rauch, A, Ostermay, S, Luther, J, Malkusch, N, Lerner, UH, Zaiss, MM, Neven, M, Wittig, R, Rauner, M, David, J-P, Bertolino, P, Zhang, CX & Tuckermann, JP 2017, 'Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis', CELL DEATH DIFFER, Jg. 24, Nr. 4, S. 672-682. https://doi.org/10.1038/cdd.2016.165

APA

Liu, P., Lee, S., Knoll, J., Rauch, A., Ostermay, S., Luther, J., Malkusch, N., Lerner, U. H., Zaiss, M. M., Neven, M., Wittig, R., Rauner, M., David, J-P., Bertolino, P., Zhang, C. X., & Tuckermann, J. P. (2017). Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis. CELL DEATH DIFFER, 24(4), 672-682. https://doi.org/10.1038/cdd.2016.165

Vancouver

Bibtex

@article{5fd1b4e0462547ab86f24df1ab299a9b,
title = "Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis",
abstract = "During osteoporosis bone formation by osteoblasts is reduced and/or bone resorption by osteoclasts is enhanced. Currently, only a few factors have been identified in the regulation of bone integrity by osteoblast-derived osteocytes. In this study, we show that specific disruption of menin, encoded by multiple endocrine neoplasia type 1 (Men1), in osteoblasts and osteocytes caused osteoporosis despite the preservation of osteoblast differentiation and the bone formation rate. Instead, an increase in osteoclast numbers and bone resorption was detected that persisted even when the deletion of Men1 was restricted to osteocytes. We demonstrate that isolated Men1-deficient osteocytes expressed numerous soluble mediators, such as C-X-C motif chemokine 10 (CXCL10), and that CXCL10-mediated osteoclastogenesis was reduced by CXCL10-neutralizing antibodies. Collectively, our data reveal a novel role for Men1 in osteocyte-osteoclast crosstalk by controlling osteoclastogenesis through the action of soluble factors. A role for Men1 in maintaining bone integrity and thereby preventing osteoporosis is proposed.",
keywords = "Journal Article",
author = "Peng Liu and Sooyeon Lee and Jeanette Knoll and Alexander Rauch and Susanne Ostermay and Julia Luther and Nicole Malkusch and Lerner, {Ulf H} and Zaiss, {Mario M} and Mona Neven and Rainer Wittig and Martina Rauner and Jean-Pierre David and Philippe Bertolino and Zhang, {Chang X} and Tuckermann, {Jan P}",
year = "2017",
month = apr,
doi = "10.1038/cdd.2016.165",
language = "English",
volume = "24",
pages = "672--682",
journal = "CELL DEATH DIFFER",
issn = "1350-9047",
publisher = "NATURE PUBLISHING GROUP",
number = "4",

}

RIS

TY - JOUR

T1 - Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis

AU - Liu, Peng

AU - Lee, Sooyeon

AU - Knoll, Jeanette

AU - Rauch, Alexander

AU - Ostermay, Susanne

AU - Luther, Julia

AU - Malkusch, Nicole

AU - Lerner, Ulf H

AU - Zaiss, Mario M

AU - Neven, Mona

AU - Wittig, Rainer

AU - Rauner, Martina

AU - David, Jean-Pierre

AU - Bertolino, Philippe

AU - Zhang, Chang X

AU - Tuckermann, Jan P

PY - 2017/4

Y1 - 2017/4

N2 - During osteoporosis bone formation by osteoblasts is reduced and/or bone resorption by osteoclasts is enhanced. Currently, only a few factors have been identified in the regulation of bone integrity by osteoblast-derived osteocytes. In this study, we show that specific disruption of menin, encoded by multiple endocrine neoplasia type 1 (Men1), in osteoblasts and osteocytes caused osteoporosis despite the preservation of osteoblast differentiation and the bone formation rate. Instead, an increase in osteoclast numbers and bone resorption was detected that persisted even when the deletion of Men1 was restricted to osteocytes. We demonstrate that isolated Men1-deficient osteocytes expressed numerous soluble mediators, such as C-X-C motif chemokine 10 (CXCL10), and that CXCL10-mediated osteoclastogenesis was reduced by CXCL10-neutralizing antibodies. Collectively, our data reveal a novel role for Men1 in osteocyte-osteoclast crosstalk by controlling osteoclastogenesis through the action of soluble factors. A role for Men1 in maintaining bone integrity and thereby preventing osteoporosis is proposed.

AB - During osteoporosis bone formation by osteoblasts is reduced and/or bone resorption by osteoclasts is enhanced. Currently, only a few factors have been identified in the regulation of bone integrity by osteoblast-derived osteocytes. In this study, we show that specific disruption of menin, encoded by multiple endocrine neoplasia type 1 (Men1), in osteoblasts and osteocytes caused osteoporosis despite the preservation of osteoblast differentiation and the bone formation rate. Instead, an increase in osteoclast numbers and bone resorption was detected that persisted even when the deletion of Men1 was restricted to osteocytes. We demonstrate that isolated Men1-deficient osteocytes expressed numerous soluble mediators, such as C-X-C motif chemokine 10 (CXCL10), and that CXCL10-mediated osteoclastogenesis was reduced by CXCL10-neutralizing antibodies. Collectively, our data reveal a novel role for Men1 in osteocyte-osteoclast crosstalk by controlling osteoclastogenesis through the action of soluble factors. A role for Men1 in maintaining bone integrity and thereby preventing osteoporosis is proposed.

KW - Journal Article

U2 - 10.1038/cdd.2016.165

DO - 10.1038/cdd.2016.165

M3 - SCORING: Journal article

C2 - 28106886

VL - 24

SP - 672

EP - 682

JO - CELL DEATH DIFFER

JF - CELL DEATH DIFFER

SN - 1350-9047

IS - 4

ER -