Expression of estrogen receptor-alpha in cells of the osteoclastic lineage

Estrogen deficiency at the menopause is associated with an increased rate of bone loss and subsequent risk of skeletal fracture. Whilst cells of the osteoblastic lineage are known to express estrogen receptors, the presence of estrogen receptors in osteoclasts remains controversial. We have examined...

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Bibliographic Details
Published in:Histochemistry and cell biology 1999-02, Vol.111 (2), p.125-133
Main Authors: Oreffo, R O, Kusec, V, Virdi, A S, Flanagan, A M, Grano, M, Zambonin-Zallone, A, Triffitt, J T
Format: Article
Language:English
Subjects:
Bone Diseases - metabolism
Bone Diseases - pathology
Bone loss
Bone marrow
Bone Marrow Cells - chemistry
Bone Marrow Cells - cytology
Bone Marrow Cells - metabolism
Bone Neoplasms - metabolism
Bone Neoplasms - pathology
Bone resorption
Breast Neoplasms - metabolism
Calcitriol
Cell Lineage
Chondroblasts
Colony-stimulating factor
Estrogen Receptor alpha
Estrogen receptors
Female
Fetuses
Gene Expression
Giant Cell Tumors - metabolism
Giant Cell Tumors - pathology
Humans
Hybridization
Hyperparathyroidism
Immunohistochemistry
In Situ Hybridization
Macrophage colony-stimulating factor
Maturation
Menopause
Monoclonal antibodies
mRNA
Muscle, Skeletal - chemistry
Muscle, Skeletal - metabolism
Osteoblasts
Osteoclastogenesis
Osteoclasts
Osteoclasts - chemistry
Osteoclasts - cytology
Osteoclasts - metabolism
Receptors, Estrogen - analysis
Receptors, Estrogen - genetics
RNA, Messenger - genetics
RNA, Messenger - metabolism
Tissue Distribution
Tumor Cells, Cultured
Tumors
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Summary:Estrogen deficiency at the menopause is associated with an increased rate of bone loss and subsequent risk of skeletal fracture. Whilst cells of the osteoblastic lineage are known to express estrogen receptors, the presence of estrogen receptors in osteoclasts remains controversial. We have examined expression of the classic estrogen receptor, estrogen receptor-alpha (ERalpha), during osteoclast differentiation. In situ mRNA hybridisation with a digoxygenin-labelled riboprobe to ERalpha mRNA, together with immunocytochemical analysis using a human ERalpha-specific monoclonal antibody demonstrated similar findings and confirmed the expression of ERalpha in chondroblasts and osteoblasts from human fetal bone and mineralising human bone marrow cultures. ERalpha expression was detected in human bone marrow cultures treated with 1,25(OH)2D3 and macrophage colony-stimulating factor and in macrophage cultures treated with 1,25(OH)2D3. However, in an in vitro model of human osteoclast formation, no ERalpha expression was observed in the osteoclasts that developed. The human preosteoclast TCG 51 cell line showed strong expression of ERalpha in contrast to the low levels observed in the more mature bone resorptive TCG 23 cell line. No expression was detectable in osteoclasts cultured from giant cell tumour of bone (GCTB) tissue or in osteoclasts in Pagetic, GCTB, or hyperparathyroid bone tissues. In conclusion, preosteoclasts express detectable levels of ERalpha, but osteoclast maturation and bone resorption is associated with loss of ERalpha expression. This indicates that ERalpha expression and regulation may play a role in osteoclast formation.
ISSN:0948-6143
1432-119X
DOI:10.1007/s004180050342