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Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects

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Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects. / Kenner, Lukas; Hoebertz, Astrid; Beil, F Timo; Beil, Timo; Keon, Niamh; Karreth, Florian; Eferl, Robert; Scheuch, Harald; Szremska, Agnieszka; Amling, Michael; Schorpp-Kistner, Marina; Angel, Peter; Wagner, Erwin F.

In: J CELL BIOL, Vol. 164, No. 4, 16.02.2004, p. 613-23.

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

Harvard

Kenner, L, Hoebertz, A, Beil, FT, Beil, T, Keon, N, Karreth, F, Eferl, R, Scheuch, H, Szremska, A, Amling, M, Schorpp-Kistner, M, Angel, P & Wagner, EF 2004, 'Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects', J CELL BIOL, vol. 164, no. 4, pp. 613-23. https://doi.org/10.1083/jcb.200308155

APA

Kenner, L., Hoebertz, A., Beil, F. T., Beil, T., Keon, N., Karreth, F., Eferl, R., Scheuch, H., Szremska, A., Amling, M., Schorpp-Kistner, M., Angel, P., & Wagner, E. F. (2004). Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects. J CELL BIOL, 164(4), 613-23. https://doi.org/10.1083/jcb.200308155

Vancouver

Kenner L, Hoebertz A, Beil FT, Beil T, Keon N, Karreth F et al. Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects. J CELL BIOL. 2004 Feb 16;164(4):613-23. https://doi.org/10.1083/jcb.200308155

Bibtex

@article{a6897799c0f646ddbbf8859ae4b2a319,
title = "Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects",
abstract = "Because JunB is an essential gene for placentation, it was conditionally deleted in the embryo proper. JunBDelta/Delta mice are born viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease. Although JunB was reported to be a negative regulator of cell proliferation, junBDelta/Delta osteoclast precursors and osteoblasts show reduced proliferation along with a differentiation defect in vivo and in vitro. Mutant osteoblasts express elevated p16(INK4a) levels, but exhibit decreased cyclin D1 and cyclin A expression. Runx2 is transiently increased during osteoblast differentiation in vitro, whereas mature osteoblast markers such as osteocalcin and bone sialoprotein are strongly reduced. To support a cell-autonomous function of JunB in osteoclasts, junB was inactivated specifically in the macrophage-osteoclast lineage. Mutant mice develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts. Thus, these data reveal a novel function of JunB as a positive regulator controlling primarily osteoblast as well as osteoclast activity.",
keywords = "Animals, Biological Markers, Bone Diseases, Metabolic, Bone and Bones, Cell Differentiation, Cell Division, Cell Lineage, Cells, Cultured, Female, Mice, Mice, Inbred C57BL, Mice, Knockout, Osteoblasts, Osteoclasts, Phenotype, Proto-Oncogene Proteins c-jun, Tissue Distribution",
author = "Lukas Kenner and Astrid Hoebertz and Beil, {F Timo} and Timo Beil and Niamh Keon and Florian Karreth and Robert Eferl and Harald Scheuch and Agnieszka Szremska and Michael Amling and Marina Schorpp-Kistner and Peter Angel and Wagner, {Erwin F}",
note = "Copyright The Rockefeller University Press",
year = "2004",
month = feb,
day = "16",
doi = "10.1083/jcb.200308155",
language = "English",
volume = "164",
pages = "613--23",
journal = "J CELL BIOL",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "4",

}

RIS

TY - JOUR

T1 - Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects

AU - Kenner, Lukas

AU - Hoebertz, Astrid

AU - Beil, F Timo

AU - Beil, Timo

AU - Keon, Niamh

AU - Karreth, Florian

AU - Eferl, Robert

AU - Scheuch, Harald

AU - Szremska, Agnieszka

AU - Amling, Michael

AU - Schorpp-Kistner, Marina

AU - Angel, Peter

AU - Wagner, Erwin F

N1 - Copyright The Rockefeller University Press

PY - 2004/2/16

Y1 - 2004/2/16

N2 - Because JunB is an essential gene for placentation, it was conditionally deleted in the embryo proper. JunBDelta/Delta mice are born viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease. Although JunB was reported to be a negative regulator of cell proliferation, junBDelta/Delta osteoclast precursors and osteoblasts show reduced proliferation along with a differentiation defect in vivo and in vitro. Mutant osteoblasts express elevated p16(INK4a) levels, but exhibit decreased cyclin D1 and cyclin A expression. Runx2 is transiently increased during osteoblast differentiation in vitro, whereas mature osteoblast markers such as osteocalcin and bone sialoprotein are strongly reduced. To support a cell-autonomous function of JunB in osteoclasts, junB was inactivated specifically in the macrophage-osteoclast lineage. Mutant mice develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts. Thus, these data reveal a novel function of JunB as a positive regulator controlling primarily osteoblast as well as osteoclast activity.

AB - Because JunB is an essential gene for placentation, it was conditionally deleted in the embryo proper. JunBDelta/Delta mice are born viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease. Although JunB was reported to be a negative regulator of cell proliferation, junBDelta/Delta osteoclast precursors and osteoblasts show reduced proliferation along with a differentiation defect in vivo and in vitro. Mutant osteoblasts express elevated p16(INK4a) levels, but exhibit decreased cyclin D1 and cyclin A expression. Runx2 is transiently increased during osteoblast differentiation in vitro, whereas mature osteoblast markers such as osteocalcin and bone sialoprotein are strongly reduced. To support a cell-autonomous function of JunB in osteoclasts, junB was inactivated specifically in the macrophage-osteoclast lineage. Mutant mice develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts. Thus, these data reveal a novel function of JunB as a positive regulator controlling primarily osteoblast as well as osteoclast activity.

KW - Animals

KW - Biological Markers

KW - Bone Diseases, Metabolic

KW - Bone and Bones

KW - Cell Differentiation

KW - Cell Division

KW - Cell Lineage

KW - Cells, Cultured

KW - Female

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Osteoblasts

KW - Osteoclasts

KW - Phenotype

KW - Proto-Oncogene Proteins c-jun

KW - Tissue Distribution

U2 - 10.1083/jcb.200308155

DO - 10.1083/jcb.200308155

M3 - SCORING: Journal article

C2 - 14769860

VL - 164

SP - 613

EP - 623

JO - J CELL BIOL

JF - J CELL BIOL

SN - 0021-9525

IS - 4

ER -