Osteoclast activity modulates B-cell development in the bone marrow

Mansour, Anna; Anginot, Adrienne; Mancini, Stéphane; Schiff, Claudine; Carle, Georges F.; Wakkach, Abdelilah; Blin-Wakkach, Claudine

doi:10.1038/cr.2011.21

Cited by 86 publications

(84 citation statements)

References 54 publications

(97 reference statements)

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“…Osteoblasts increase after ovariectomy in response to increased bone resorption, a phenomenon known as coupling (20). Moreover, osteoblasts provide factors such as IL-7 and CXCL-12 that support B cell development (21)(22)(23)(24). Consistent with the idea that the failure to increase B cells was due to reduced support by osteoblast-lineage cells, IL-7 mRNA in bone was increased by ovariectomy in Tnfsf11 f/f but not Tnfsf11 ⌬Ot mice (Fig.…”

Section: Osteocyte Rankl Is Required For Ovariectomy-induced Bonesupporting

confidence: 71%

“…Many of these previous studies include evidence that osteoblast-lineage cells support B cell development by expressing IL-7 and CXCL-12 (22,23,32). We found that IL-7 and CXCL-12 mRNAs were elevated by ovariectomy in control mice but not in Tnfsf11 ⌬Ot mice.…”

Section: Discussionsupporting

confidence: 51%

“…In addition, suppression of PTH receptor signaling specifically in osteoblasts reduces B cell number (22). Perhaps most relevant to the current work, suppression of bone remodeling by administration of bisphosphonates is sufficient to reduce the number of osteoblasts on the bone surface and the number of B cells in the bone marrow of mice (23,33).…”

Section: Discussionmentioning

confidence: 81%

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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

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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.

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Section: Osteocyte Rankl Is Required For Ovariectomy-induced Bonesupporting

confidence: 71%

Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 81%

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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

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“…This is probably related to the respective roles proposed for these niches; the endosteal niche is supposed to be a long-term storage niche containing the most dormant HSCs, and the vascular niche is supposed to contain self-renewing and mobilized HSCs. 2 Interestingly, in adults, HSCs are weakly affected by OBL ablation 10 or by the blockade of OCL activity 7 in contrast with what we observed in newborn mice. 6 These observations suggest that the mechanisms involved in the initial establishment of the niche in the BM at birth are distinct from those involved in its maintenance and regulation in adults.…”

contrasting

confidence: 55%

Role of osteoclasts in the hematopoietic stem cell niche formation

Mansour¹,

Wakkach²,

Blin-Wakkach³

2012

Cell Cycle

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“…It has been shown that the inhibition of osteoclast function reduces the number of BM HSCs in vivo [28,29] and increases the number of HSCs in the spleen [30]. Others have, however, reported that osteoclasts are either dispensable for HSC maintenance and mobilization [31][32][33], or that they affect the HSC niche only indirectly, through an effect on osteoblast differentiation [25], while at the same time actively modulating B-cell development [34]. Taken together, this indicates that osteoclasts are important for the homeostasis of the BM microenvironment.…”

Section: Introductionmentioning

confidence: 99%