Universität zu Köln

Gu, Ran, Santos, Leilani L., Ngo, Devi, Fan, HuaPeng, Singh, Preetinder P., Fingerle-Rowson, Gunter, Bucala, Richard, Xu, Jiake, Quinn, Julian M. W. and Morand, Eric F. (2015). Macrophage migration inhibitory factor is essential for osteoclastogenic mechanisms in vitro and in vivo mouse model of arthritis. Cytokine, 72 (2). S. 135 - 146. LONDON: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. ISSN 1096-0023

Full text not available from this repository.

Abstract

Macrophage migration inhibitory factor (MIF) enhances activation of leukocytes, endothelial cells and fibroblast-like synoviocytes (FLS), thereby contributing to the pathogenesis of rheumatoid arthritis (RA). A MIF promoter polymorphism in RA patients resulted in higher serum MIF concentration and worsens bone erosion; controversially current literature reported an inhibitory role of MIF in osteoclast formation. The controversial suggested that the prease role of MIF and its putative receptor CD74 in osteoclastogenesis and RA bone erosion, mediated by locally formed osteoclasts in response to receptor activator of NF-kappa B ligand (RANKL), is unclear. We reported that in an in vivo K/BxN serum transfer arthritis, reduced clinical and histological arthritis in MIF-/- and CD74(-/-) mice were accompanied by a virtual absence of osteoclasts at the synovium-bone interface and reduced osteoclast-related gene expression. Furthermore, in vitro osteoclast formation and osteoclast-related gene expression were significantly reduced in MIF-/- cells via decreasing RANKL-induced phosphorylation of NF-kappa B-p65 and ERK1/2. This was supported by a similar reduction of osteoclastogenesis observed in CD74(-/-) cells. Furthermore, a MIF blockade reduced RANKL-induced osteoclastogeriesis via deregulating RANKL-mediated NF-kappa B and NFATc1 transcription factor activation. These data indicate that MIF and CD74 facilitate RANKL-induced osteoclastogenesis, and suggest that MIF contributes directly to bone erosion, as well as inflammation, in RA. (C) 2014 Elsevier Ltd. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Gu, Ran UNSPECIFIED UNSPECIFIED UNSPECIFIED Santos, Leilani L. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ngo, Devi UNSPECIFIED UNSPECIFIED UNSPECIFIED Fan, HuaPeng UNSPECIFIED UNSPECIFIED UNSPECIFIED Singh, Preetinder P. UNSPECIFIED UNSPECIFIED UNSPECIFIED Fingerle-Rowson, Gunter UNSPECIFIED UNSPECIFIED UNSPECIFIED Bucala, Richard UNSPECIFIED UNSPECIFIED UNSPECIFIED Xu, Jiake UNSPECIFIED UNSPECIFIED UNSPECIFIED Quinn, Julian M. W. UNSPECIFIED UNSPECIFIED UNSPECIFIED Morand, Eric F. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-403654
DOI:	10.1016/j.cyto.2014.11.015
Journal or Publication Title:	Cytokine
Volume:	72
Number:	2
Page Range:	S. 135 - 146
Date:	2015
Publisher:	ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Place of Publication:	LONDON
ISSN:	1096-0023
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language NF-KAPPA-B; INDUCED BONE LOSS; RHEUMATOID-ARTHRITIS; FACTOR MIF; RECEPTOR ACTIVATOR; MAP KINASE; PROINFLAMMATORY FUNCTION; SIGNALING PATHWAYS; DEFICIENT MICE; LIGAND RANKL Multiple languages Biochemistry & Molecular Biology; Cell Biology; Immunology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/40365