M‐CSF Priming of Osteoclast Precursors Can Cause Osteoclastogenesis‐Insensitivity, Which Can Be Prevented and Overcome on Bone. Issue 1 (January 2015)
- Record Type:
- Journal Article
- Title:
- M‐CSF Priming of Osteoclast Precursors Can Cause Osteoclastogenesis‐Insensitivity, Which Can Be Prevented and Overcome on Bone. Issue 1 (January 2015)
- Main Title:
- M‐CSF Priming of Osteoclast Precursors Can Cause Osteoclastogenesis‐Insensitivity, Which Can Be Prevented and Overcome on Bone
- Authors:
- De vries, Teun J.
Schoenmaker, Ton
Aerts, David
Grevers, Lilyanne C.
Souza, Pedro P.C.
Nazmi, Kamran
van de Wiel, Mark
Ylstra, Bauke
Lent, Peter L. Van
Leenen, Pieter J.M.
Everts, Vincent - Abstract:
- <abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="jcp24702-sec-0001" sec-type="section"> <p>Osteoclasts and macrophages share progenitors that must receive decisive lineage signals driving them into their respective differentiation routes. Macrophage colony stimulation factor M‐CSF is a common factor; bone is likely the stimulus for osteoclast differentiation. To elucidate the effect of both, shared mouse bone marrow precursor myeloid blast was pre‐cultured with M‐CSF on plastic and on bone. M‐CSF priming prior to stimulation with M‐CSF and osteoclast differentiation factor RANKL resulted in a complete loss of osteoclastogenic potential without bone. Such M‐CSF primed cells expressed the receptor RANK, but lacked the crucial osteoclastogenic transcription factor NFATc1. This coincided with a steeply decreased expression of osteoclast genes TRACP and DC‐STAMP, but an increased expression of the macrophage markers F4/80 and CD11b. Compellingly, M‐CSF priming on bone accelerated the osteoclastogenic potential: M‐CSF primed cells that had received only one day M‐CSF and RANKL and were grown on bone already expressed an array of genes that are associated with osteoclast differentiation and these cells differentiated into osteoclasts within 2 days. Osteoclastogenesis‐insensitive precursors grown in the absence of bone regained their osteoclastogenic potential when transferred to bone. This implies that adhesion to bone dictates the fate of osteoclast<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="jcp24702-sec-0001" sec-type="section"> <p>Osteoclasts and macrophages share progenitors that must receive decisive lineage signals driving them into their respective differentiation routes. Macrophage colony stimulation factor M‐CSF is a common factor; bone is likely the stimulus for osteoclast differentiation. To elucidate the effect of both, shared mouse bone marrow precursor myeloid blast was pre‐cultured with M‐CSF on plastic and on bone. M‐CSF priming prior to stimulation with M‐CSF and osteoclast differentiation factor RANKL resulted in a complete loss of osteoclastogenic potential without bone. Such M‐CSF primed cells expressed the receptor RANK, but lacked the crucial osteoclastogenic transcription factor NFATc1. This coincided with a steeply decreased expression of osteoclast genes TRACP and DC‐STAMP, but an increased expression of the macrophage markers F4/80 and CD11b. Compellingly, M‐CSF priming on bone accelerated the osteoclastogenic potential: M‐CSF primed cells that had received only one day M‐CSF and RANKL and were grown on bone already expressed an array of genes that are associated with osteoclast differentiation and these cells differentiated into osteoclasts within 2 days. Osteoclastogenesis‐insensitive precursors grown in the absence of bone regained their osteoclastogenic potential when transferred to bone. This implies that adhesion to bone dictates the fate of osteoclast precursors. Common macrophage‐osteoclast precursors may become insensitive to differentiate into osteoclasts and regain osteoclastogenesis when bound to bone or when in the vicinity of bone. J. Cell. Physiol. 229: 210–225, 2014. © 2014 Wiley Periodicals, Inc.</p> </sec> </abstract> … (more)
- Is Part Of:
- Journal of cellular physiology. Volume 230:Issue 1(2015:Jan.)
- Journal:
- Journal of cellular physiology
- Issue:
- Volume 230:Issue 1(2015:Jan.)
- Issue Display:
- Volume 230, Issue 1 (2015)
- Year:
- 2015
- Volume:
- 230
- Issue:
- 1
- Issue Sort Value:
- 2015-0230-0001-0000
- Page Start:
- 210
- Page End:
- 225
- Publication Date:
- 2015-01
- Subjects:
- Physiology -- Periodicals
Cell physiology -- Periodicals
571.6 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4652 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jcp.24702 ↗
- Languages:
- English
- ISSNs:
- 0021-9541
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4955.020000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 4083.xml