M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.

Macrophage-CSF (M-CSF) is critical for osteoclast (OC) differentiation and is reported to enhance mature OC survival and motility. However, its role in the regulation of bone resorption, the main function of OCs, has not been well characterised. To address this we analysed short-term cultures of ful...

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Autores principales:	Jason M Hodge, Fiona M Collier, Nathan J Pavlos, Mark A Kirkland, Geoffrey C Nicholson
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5e35af53f8344c7fb260abc9b243bfd3
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spelling	oai:doaj.org-article:5e35af53f8344c7fb260abc9b243bfd32021-11-18T06:51:00ZM-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.1932-620310.1371/journal.pone.0021462https://doaj.org/article/5e35af53f8344c7fb260abc9b243bfd32011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21738673/?tool=EBIhttps://doaj.org/toc/1932-6203Macrophage-CSF (M-CSF) is critical for osteoclast (OC) differentiation and is reported to enhance mature OC survival and motility. However, its role in the regulation of bone resorption, the main function of OCs, has not been well characterised. To address this we analysed short-term cultures of fully differentiated OCs derived from human colony forming unit-granulocyte macrophages (CFU-GM). When cultured on dentine, OC survival was enhanced by M-CSF but more effectively by receptor activator of NFκB ligand (RANKL). Resorption was entirely dependent on the presence of RANKL. Co-treatment with M-CSF augmented RANKL-induced resorption in a concentration-dependent manner with a (200-300%) stimulation at 25 ng/mL, an effect observed within 4-6 h. M-CSF co-treatment also increased number of resorption pits and F-actin sealing zones, but not the number of OCs or pit size, indicating stimulation of the proportion of OCs activated. M-CSF facilitated RANKL-induced activation of c-fos and extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, but not NFκB nor nuclear factor of activated T-cells, cytoplasmic-1 (NFATc1). The mitogen-activated protein kinase kinase (MEK) 1 inhibitor PD98059 partially blocked augmentation of resorption by M-CSF. Our results reveal a previously unidentified role of M-CSF as a potent stimulator of mature OC resorbing activity, possibly mediated via ERK upstream of c-fos.Jason M HodgeFiona M CollierNathan J PavlosMark A KirklandGeoffrey C NicholsonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 6, p e21462 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jason M Hodge Fiona M Collier Nathan J Pavlos Mark A Kirkland Geoffrey C Nicholson M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.
description	Macrophage-CSF (M-CSF) is critical for osteoclast (OC) differentiation and is reported to enhance mature OC survival and motility. However, its role in the regulation of bone resorption, the main function of OCs, has not been well characterised. To address this we analysed short-term cultures of fully differentiated OCs derived from human colony forming unit-granulocyte macrophages (CFU-GM). When cultured on dentine, OC survival was enhanced by M-CSF but more effectively by receptor activator of NFκB ligand (RANKL). Resorption was entirely dependent on the presence of RANKL. Co-treatment with M-CSF augmented RANKL-induced resorption in a concentration-dependent manner with a (200-300%) stimulation at 25 ng/mL, an effect observed within 4-6 h. M-CSF co-treatment also increased number of resorption pits and F-actin sealing zones, but not the number of OCs or pit size, indicating stimulation of the proportion of OCs activated. M-CSF facilitated RANKL-induced activation of c-fos and extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, but not NFκB nor nuclear factor of activated T-cells, cytoplasmic-1 (NFATc1). The mitogen-activated protein kinase kinase (MEK) 1 inhibitor PD98059 partially blocked augmentation of resorption by M-CSF. Our results reveal a previously unidentified role of M-CSF as a potent stimulator of mature OC resorbing activity, possibly mediated via ERK upstream of c-fos.
format	article
author	Jason M Hodge Fiona M Collier Nathan J Pavlos Mark A Kirkland Geoffrey C Nicholson
author_facet	Jason M Hodge Fiona M Collier Nathan J Pavlos Mark A Kirkland Geoffrey C Nicholson
author_sort	Jason M Hodge
title	M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.
title_short	M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.
title_full	M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.
title_fullStr	M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.
title_full_unstemmed	M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.
title_sort	m-csf potently augments rankl-induced resorption activation in mature human osteoclasts.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/5e35af53f8344c7fb260abc9b243bfd3
work_keys_str_mv	AT jasonmhodge mcsfpotentlyaugmentsranklinducedresorptionactivationinmaturehumanosteoclasts AT fionamcollier mcsfpotentlyaugmentsranklinducedresorptionactivationinmaturehumanosteoclasts AT nathanjpavlos mcsfpotentlyaugmentsranklinducedresorptionactivationinmaturehumanosteoclasts AT markakirkland mcsfpotentlyaugmentsranklinducedresorptionactivationinmaturehumanosteoclasts AT geoffreycnicholson mcsfpotentlyaugmentsranklinducedresorptionactivationinmaturehumanosteoclasts
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M-CSF potently augments RANKL-induced resorption activation in mature human osteoclasts.

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