Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Lipopolysaccharide supports survival and fusion of preosteoclasts independent of TNF-alpha, IL-1, and RANKL
Autore:
Suda, K; Woo, JT; Takami, M; Sexton, PM; Nagai, K;
Indirizzi:
Tokyo Inst Technol, Dept Bioengn, Midori Ku, Yokohama, Kanagawa 2268501, Japan Tokyo Inst Technol Yokohama Kanagawa Japan 2268501 anagawa 2268501, Japan Univ Melbourne, Howard Florey Inst Expt Physiol & Med, Parkville, Vic 3052, Australia Univ Melbourne Parkville Vic Australia 3052 arkville, Vic 3052, Australia
Titolo Testata:
JOURNAL OF CELLULAR PHYSIOLOGY
fascicolo: 1, volume: 190, anno: 2002,
pagine: 101 - 108
SICI:
0021-9541(200201)190:1<101:LSSAFO>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; COLONY-STIMULATING FACTOR; OSTEOCLAST DIFFERENTIATION; OSTEOBLASTIC CELLS; IN-VITRO; RECEPTOR; ACTIVATION; MICE; INTERLEUKIN-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Nagai, K Tokyo Inst Technol, Dept Bioengn, Midori Ku, 4259 Nagatsuta Cho, Yokohama,Kanagawa 2268501, Japan Tokyo Inst Technol 4259 Nagatsuta Cho Yokohama Kanagawa Japan 2268501
Citazione:
K. Suda et al., "Lipopolysaccharide supports survival and fusion of preosteoclasts independent of TNF-alpha, IL-1, and RANKL", J CELL PHYS, 190(1), 2002, pp. 101-108

Abstract

Lipopolysaccharide (LPS), a cell component of Gram-negative bacteria, is apathogen of inflammatory bone loss. To examine the effects of LPS on the survival and fusion of osteoclasts, mononuclear osteoclasts (preosteoclasts,pOCs) were collected from a mouse co-culture system and cultured in the presence or absence of LPS. Most pOCs died within 24 h in the absence of any stimulus. LPS as well as receptor activator of NF-kappaB ligand (RANKL) supported the survival of pOCs, and induced their fusion to form multinucleated cells (MNCs). Like authentic osteoclasts, MNCs induced by LPS expressed calcitonin receptors, and formed actin rings on culture plates. LPS-induced MNC formation in pOC cultures was observed even in the presence of osteoprotegerin and interleukin (IL)-1-receptor antagonists. MNC formation was alsostimulated by LPS in pOC cultures prepared from tumor necrosis factor (TNF)-receptor-1 or TNF-receptor-II deficient mice. LPS induced the degradationof I kappaB in pOCs within 20 min. Lactacystin, an inhibitor of NF-kappaB activation, and wortmannin, an inhibitor of phosphatidylinositol-3 kinase, strongly inhibited LPS-induced MNC formation in pOC cultures. LPS induced pit-forming activity of pOCs in the presence of macrophage-colony stimulating factor (M-CSF). These findings suggest that LPS stimulates the survival and fusion of pOCs, independent of RANKL, IL-1 or TNF-alpha action. Activation of NF-kappaB and phosphatidylinositol-3 kinase appeared to be involved in LPS-induced effects on pOCs. These observations suggest that LPS is involved directly in inflammatory bone loss, and also indirectly through the production of LPS-induced host factors such as IL-1 and TNF-alpha. (C) 2002 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 16:37:23