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Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts. / Sørensen, M G; Henriksen, K; Dziegiel, Morten Hanefeld; Tankó, L B; Karsdal, M A.

I: D N A and Cell Biology, Bind 25, Nr. 8, 08.2006, s. 475-83.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Sørensen, MG, Henriksen, K, Dziegiel, MH, Tankó, LB & Karsdal, MA 2006, 'Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts', D N A and Cell Biology, bind 25, nr. 8, s. 475-83. https://doi.org/10.1089/dna.2006.25.475

APA

Sørensen, M. G., Henriksen, K., Dziegiel, M. H., Tankó, L. B., & Karsdal, M. A. (2006). Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts. D N A and Cell Biology, 25(8), 475-83. https://doi.org/10.1089/dna.2006.25.475

Vancouver

Sørensen MG, Henriksen K, Dziegiel MH, Tankó LB, Karsdal MA. Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts. D N A and Cell Biology. 2006 aug;25(8):475-83. https://doi.org/10.1089/dna.2006.25.475

Author

Sørensen, M G ; Henriksen, K ; Dziegiel, Morten Hanefeld ; Tankó, L B ; Karsdal, M A. / Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts. I: D N A and Cell Biology. 2006 ; Bind 25, Nr. 8. s. 475-83.

Bibtex

@article{e9228155046c4a6a84d5c69a53e0c21b,
title = "Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts",
abstract = "Estrogen deficiency arising with the menopause promotes marked acceleration of bone resorption, which can be restored by hormone replacement therapy. The inhibitory effects of estrogen seem to involve indirect cytokine- mediated effects via supporting bone marrow cells, but direct estrogen-receptor mediated effects on the bone-resorbing osteoclasts have also been proposed. Little information is available on whether estrogens modulate human osteoclastogenesis or merely inhibit the functional activity of osteoclasts. To clarify whether estrogens directly modulate osteoclastic activities human CD14+ monocytes were cultured in the presence of M-CSF and RANKL to induce osteoclast differentiation. Addition of 0.1-10 nM 17beta-estradiol to differentiating osteoclasts resulted in a dose-dependent reduction in tartrate resistant acid phosphatase (TRACP) activity reaching 60% at 0.1 nM. In addition, 17beta-estradiol inhibited bone resorption, as measured by the release of the C-terminal crosslinked telopeptide (CTX), by 60% at 0.1 nM, but had no effect on the overall cell viability. In contrast to the results obtained with differentiating osteoclasts, addition of 17beta-estradiol (0.001-10 nM) to mature osteoclasts did not affect bone resorption or TRACP activity. We investigated expression of the estrogen receptors, using immunocytochemistry and Western blotting. We found that ER-alpha is expressed in osteoclast precursors, whereas ER- beta is expressed at all stages, indicating that the inhibitory effect of estrogen on osteoclastogenesis is mediated by ER-alpha for the major part. In conclusion, these results suggest that the in vivo effects of estrogen are mediated by reduction of osteoclastogenesis rather than direct inhibition of the resorptive activity of mature osteoclasts.",
keywords = "Blotting, Western, Bone Resorption, Estradiol, Estrogen Receptor alpha, Estrogen Receptor beta, Humans, Immunohistochemistry, Osteoclasts",
author = "S{\o}rensen, {M G} and K Henriksen and Dziegiel, {Morten Hanefeld} and Tank{\'o}, {L B} and Karsdal, {M A}",
year = "2006",
month = aug,
doi = "10.1089/dna.2006.25.475",
language = "English",
volume = "25",
pages = "475--83",
journal = "D N A and Cell Biology",
issn = "1044-5498",
publisher = "Mary AnnLiebert, Inc. Publishers",
number = "8",

}

RIS

TY - JOUR

T1 - Estrogen directly attenuates human osteoclastogenesis, but has no effect on resorption by mature osteoclasts

AU - Sørensen, M G

AU - Henriksen, K

AU - Dziegiel, Morten Hanefeld

AU - Tankó, L B

AU - Karsdal, M A

PY - 2006/8

Y1 - 2006/8

N2 - Estrogen deficiency arising with the menopause promotes marked acceleration of bone resorption, which can be restored by hormone replacement therapy. The inhibitory effects of estrogen seem to involve indirect cytokine- mediated effects via supporting bone marrow cells, but direct estrogen-receptor mediated effects on the bone-resorbing osteoclasts have also been proposed. Little information is available on whether estrogens modulate human osteoclastogenesis or merely inhibit the functional activity of osteoclasts. To clarify whether estrogens directly modulate osteoclastic activities human CD14+ monocytes were cultured in the presence of M-CSF and RANKL to induce osteoclast differentiation. Addition of 0.1-10 nM 17beta-estradiol to differentiating osteoclasts resulted in a dose-dependent reduction in tartrate resistant acid phosphatase (TRACP) activity reaching 60% at 0.1 nM. In addition, 17beta-estradiol inhibited bone resorption, as measured by the release of the C-terminal crosslinked telopeptide (CTX), by 60% at 0.1 nM, but had no effect on the overall cell viability. In contrast to the results obtained with differentiating osteoclasts, addition of 17beta-estradiol (0.001-10 nM) to mature osteoclasts did not affect bone resorption or TRACP activity. We investigated expression of the estrogen receptors, using immunocytochemistry and Western blotting. We found that ER-alpha is expressed in osteoclast precursors, whereas ER- beta is expressed at all stages, indicating that the inhibitory effect of estrogen on osteoclastogenesis is mediated by ER-alpha for the major part. In conclusion, these results suggest that the in vivo effects of estrogen are mediated by reduction of osteoclastogenesis rather than direct inhibition of the resorptive activity of mature osteoclasts.

AB - Estrogen deficiency arising with the menopause promotes marked acceleration of bone resorption, which can be restored by hormone replacement therapy. The inhibitory effects of estrogen seem to involve indirect cytokine- mediated effects via supporting bone marrow cells, but direct estrogen-receptor mediated effects on the bone-resorbing osteoclasts have also been proposed. Little information is available on whether estrogens modulate human osteoclastogenesis or merely inhibit the functional activity of osteoclasts. To clarify whether estrogens directly modulate osteoclastic activities human CD14+ monocytes were cultured in the presence of M-CSF and RANKL to induce osteoclast differentiation. Addition of 0.1-10 nM 17beta-estradiol to differentiating osteoclasts resulted in a dose-dependent reduction in tartrate resistant acid phosphatase (TRACP) activity reaching 60% at 0.1 nM. In addition, 17beta-estradiol inhibited bone resorption, as measured by the release of the C-terminal crosslinked telopeptide (CTX), by 60% at 0.1 nM, but had no effect on the overall cell viability. In contrast to the results obtained with differentiating osteoclasts, addition of 17beta-estradiol (0.001-10 nM) to mature osteoclasts did not affect bone resorption or TRACP activity. We investigated expression of the estrogen receptors, using immunocytochemistry and Western blotting. We found that ER-alpha is expressed in osteoclast precursors, whereas ER- beta is expressed at all stages, indicating that the inhibitory effect of estrogen on osteoclastogenesis is mediated by ER-alpha for the major part. In conclusion, these results suggest that the in vivo effects of estrogen are mediated by reduction of osteoclastogenesis rather than direct inhibition of the resorptive activity of mature osteoclasts.

KW - Blotting, Western

KW - Bone Resorption

KW - Estradiol

KW - Estrogen Receptor alpha

KW - Estrogen Receptor beta

KW - Humans

KW - Immunohistochemistry

KW - Osteoclasts

U2 - 10.1089/dna.2006.25.475

DO - 10.1089/dna.2006.25.475

M3 - Journal article

C2 - 16907645

VL - 25

SP - 475

EP - 483

JO - D N A and Cell Biology

JF - D N A and Cell Biology

SN - 1044-5498

IS - 8

ER -

ID: 47556704