Artigo
M-CSF Priming of Osteoclast Precursors Can Cause Osteoclastogenesis-Insensitivity, Which Can be Prevented and Overcome on Bone
Registro en:
Journal Of Cellular Physiology. Hoboken: Wiley-blackwell, v. 230, n. 1, p. 210-225, 2015.
0021-9541
10.1002/jcp.24702
WOS:000342762200020
Autor
De Vries, Teun J.
Schoenmaker, Ton
Aerts, David
Grevers, Lilyanne C.
Souza, Pedro P. C. [UNESP]
Nazmi, Kamran
Van De Wiel, Mark A.
Ylstra, Bauke
Van Lent, Peter L.
Leenen, Pieter J. M.
Everts, Vincent
Resumen
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. (c) 2014 Wiley Periodicals, Inc. Vrije Univ Amsterdam, Univ Amsterdam, MOVE Res Inst, Dept Periodontol, NL-1081 LA Amsterdam, Netherlands Vrije Univ Amsterdam, Univ Amsterdam, MOVE Res Inst, Dept Oral Cell Biol, NL-1081 LA Amsterdam, Netherlands Radboud Univ Nijmegen, Nijmegen Med Ctr, Dept Reumatol Res & Therapeut, NL-6525 ED Nijmegen, Netherlands Sao Paulo State Univ, Araraquara Sch Dent, Dept Physiol & Pathol, Araraquara, Brazil Univ Amsterdam, Acad Ctr Dent Amsterdam ACTA, Dept Oral Biochem, NL-1081 LA Amsterdam, Netherlands Vrije Univ Amsterdam, MOVE Res Inst, NL-1081 LA Amsterdam, Netherlands Vrije Univ Amsterdam, Med Ctr, Dept Epidemiol & Biostat, NL-1081 LA Amsterdam, Netherlands Vrije Univ Amsterdam, Dept Math, NL-1081 LA Amsterdam, Netherlands Vrije Univ Amsterdam, Med Ctr, Dept Pathol, NL-1081 LA Amsterdam, Netherlands Vrije Univ Amsterdam, Med Ctr, Microarray Facil, NL-1081 LA Amsterdam, Netherlands Univ Med Ctr, Erasmus MC, Dept Immunol, Rotterdam, Netherlands Sao Paulo State Univ, Araraquara Sch Dent, Dept Physiol & Pathol, Araraquara, Brazil