Estrogen receptor-α in osteocytes is important for trabecular bone formation in male mice

Windahl, Sara H; Börjesson, Anna; Farman, Helen H; Engdahl, Cecilia; Movérare‐Skrtic, Sofia; Sjögren, Klara; Lagerquist, Marie K; Kindblom, Jenny M.; Koskela, Antti; Tuukkanen, Juha; Pajevic, Paola Divieti; Feng, Jian Q.; Dahlman-Wright, Karin; Antonson, Per; Gustafsson, Jan‐Åke; Ohlsson, Claes

doi:10.1073/pnas.1220811110

Cited by 122 publications

(130 citation statements)

References 41 publications

Supporting

Mentioning

114

Contrasting

Order By: Relevance

“…Thus RANKL expression by osteocytes is permissive for the increase in osteoclast number and did not appear to be a direct target of estrogen. Consistent with this finding, deletion of ER␣ from osteocytes has no effect on osteoclast number (26,27). We and others have shown that the amount of soluble RANKL protein in bone marrow supernatants does increase with either estrogen or androgen deficiency (12,28,29).…”

Section: Discussionsupporting

confidence: 52%

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

Fujiwara

Piemontese

Liu

et al. 2016

Journal of Biological Chemistry

View full text Add to dashboard Cite

Edited by Luke O'NeillThe cytokine receptor activator of NFB ligand (RANKL) produced by osteocytes is essential for osteoclast formation in cancellous bone under physiological conditions, and RANKL production by B lymphocytes is required for the bone loss caused by estrogen deficiency. Here, we examined whether RANKL produced by osteocytes is also required for the bone loss caused by estrogen deficiency. Mice lacking RANKL in osteocytes were protected from the increase in osteoclast number and the bone loss caused by ovariectomy. Moreover, these mice did not exhibit the increase in bone marrow B lymphocytes caused by ovariectomy that occurred in control littermates. Deletion of estrogen receptor ␣ from B cells did not alter B cell number or bone mass and did not alter the response to ovariectomy. In addition, lineage-tracing studies demonstrated that B cells do not act as osteoclast progenitors in estrogen-replete or estrogen-deficient mice. Taken together, these results demonstrate that RANKL expressed by osteocytes is required for the bone loss as well as the increase in B cell number caused by estrogen deficiency. Moreover, they suggest that estrogen control of B cell number is indirect via osteocytes and that the increase in bone marrow B cells may be a necessary component of the cascade of events that lead to cancellous bone loss during estrogen deficiency. However, the role of B cells is not to act as osteoclast progenitors but may be to act as osteoclast support cells.

show abstract

Section: Discussionsupporting

confidence: 52%

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

Fujiwara

Piemontese

Liu

et al. 2016

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Two different laboratories developed and characterized this animal model. In line with ERa deletion in mature osteoblasts [55], females with ERa deletion in osteocytes do not exhibit bone loss [62]. According to Windahl et al, only males with specific ERa deletion in osteocytes display a substantial reduction in femoral, tibiae and vertebral trabecular bone volume.…”

Section: Actions Of Era In Osteoblasts Precursors Osteoblasts and Osmentioning

confidence: 97%

The Role of Estrogen Receptor in Bone Cells

Millán

2015

Clinic Rev Bone Miner Metab

View full text Add to dashboard Cite

Estrogen is an essential regulator of the skeleton homeostasis during both childhood and adulthood. As a matter of fact, estrogens and selective estrogen receptor modulators are considered essential treatment tools by clinicians to prevent bone fractures in postmenopausal women. All these observations promote a great interest in discovering the mechanisms by which estrogens protect bone. Over the past years, research performed from several groups has established that the osteoprotective effects of estrogens are due to both direct actions on bone cells and indirect effects mediated through bone marrow cells. Experiments performed in humans and animals, in which estrogen receptor deletion was specifically carried out in different bone cells, have allowed unraveling some aspects of the estrogen actions on bone through these cells. This review highlights the current knowledge about the role of estrogens in the RANKL/OPG system, as well as their role in different bone cells and bone marrow cells.

show abstract

“…11,14,15,19,20 Alternatively, some researchers have specified a volume (for example, 2 mm) centred at the midline, 8 or they have used the growth plate as a landmark. 7,21,22 As the mid-region is sparsely populated with trabecular bone, and the bone volume density is inhomogeneously distributed throughout the vertebral body, it is recommended to analyse the entire volume unless the study question gives cause to focus on a specific subvolume. Corrects for the absorption of lower-energy X-ray on the outside of the specimen 10-25% (optimal setting should be determined empirically)…”

Section: Trabecular Bonementioning

confidence: 99%

Quantitative analysis of bone and soft tissue by micro-computed tomography: applications to ex vivo and in vivo studies

Campbell¹,

Sophocleous²

2014

BoneKEy Reports

124

106

View full text Add to dashboard Cite

Micro-computed tomography (micro-CT) is a high-resolution imaging modality that is capable of analysing bone structure with a voxel size on the order of 10 mm. With the development of in vivo micro-CT, where disease progression and treatment can be monitored in a living animal over a period of time, this modality has become a standard tool for preclinical assessment of bone architecture during disease progression and treatment. For meaningful comparison between micro-CT studies, it is essential that the same parameters for data acquisition and analysis methods be used. This protocol outlines the common procedures that are currently used for sample preparation, scanning, reconstruction and analysis in micro-CTstudies. Scan and analysis methods for trabecular and cortical bone are covered for the femur, tibia, vertebra and the full neonate body of small rodents. The analysis procedures using the software provided by ScancoMedical and Bruker are discussed, and the routinely used bone architectural parameters are outlined. This protocol also provides a section dedicated to in vivo scanning and analysis, which covers the topics of anaesthesia, radiation dose and image registration. Because of the expanding research using micro-CT to study other skeletal sites, as well as soft tissues, we also provide a review of current techniques to examine the skull and mandible, adipose tissue, vasculature, tumour severity and cartilage. Lists of recommended further reading and literature references are included to provide the reader with more detail on the methods described.

show abstract

Estrogen receptor-α in osteocytes is important for trabecular bone formation in male mice

Cited by 122 publications

References 41 publications

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

The Role of Estrogen Receptor in Bone Cells

Quantitative analysis of bone and soft tissue by micro-computed tomography: applications to ex vivo and in vivo studies

Contact Info

Product

Resources

About