PMID- 15135808
OWN - NLM
STAT- MEDLINE
DCOM- 20041230
LR  - 20061115
IS  - 1043-4666 (Print)
IS  - 1043-4666 (Linking)
VI  - 26
IP  - 3
DP  - 2004 May 7
TI  - Human interleukin-1-induced murine osteoclastogenesis is dependent on RANKL, but 
      independent of TNF-alpha.
PG  - 138-44
AB  - Although interleukin-1 (IL-1) has been implicated in the pathogenesis of 
      inflammatory osteolysis, the means by which it recruits osteoclasts and promotes 
      bone destruction are largely unknown. Recently, a cytokine-driven, stromal 
      cell-free mouse osteoclastogenesis model was established. A combination of 
      macrophage colony stimulating factor (M-CSF) and receptor activator of NFkappaB 
      ligand (RANKL) was proven to be sufficient in inducing differentiation of bone 
      marrow hematopoietic precursor cells to bone-resorbing osteoclasts in the absence 
      of stromal cells or osteoblasts. This study utilizes this model to examine the 
      impact of human IL-1beta on in vitro osteoclastogenesis of bone marrow progenitor 
      cells. We found that osteoclast precursor cells failed to undergo 
      osteoclastogenesis when treated with IL-1 alone. In contrast, IL-1 dramatically 
      up-regulated osteoclastogenesis by 2.5- to 4-folds in the presence of RANKL and 
      M-CSF. The effect can be significantly blocked by IL-1 receptor antagonist (p < 
      0.01). Tumor necrosis factor-alpha (TNF-alpha) was undetectable in the culture 
      medium of differentiating osteoclasts induced by IL-1. Adding exogenous TNF-alpha 
      neutralizing antibody had no influence on the IL-1-induced effect as well. These 
      results show that in the absence of stromal cells, IL-1 exacerbates 
      osteoclastogenesis by cooperating with RANKL and M-CSF, while TNF-alpha is not 
      involved in this IL-1-stimulated osteoclast differentiation pathway.
CI  - Copyright 2004 Elsevier Ltd.
FAU - Ma, Ting
AU  - Ma T
AD  - Department of Orthopaedic Surgery, Stanford University School of Medicine, 300 
      Pasteur Drive, Edwards Building, R144, Stanford, CA 94305-5341, USA.
FAU - Miyanishi, Keita
AU  - Miyanishi K
FAU - Suen, Andrew
AU  - Suen A
FAU - Epstein, Noah J
AU  - Epstein NJ
FAU - Tomita, Tetsuya
AU  - Tomita T
FAU - Smith, R Lane
AU  - Smith RL
FAU - Goodman, Stuart B
AU  - Goodman SB
LA  - eng
PT  - Journal Article
PL  - England
TA  - Cytokine
JT  - Cytokine
JID - 9005353
RN  - 0 (Carrier Proteins)
RN  - 0 (Interleukin-1)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (RANK Ligand)
RN  - 0 (Receptor Activator of Nuclear Factor-kappa B)
RN  - 0 (TNFRSF11A protein, human)
RN  - 0 (TNFSF11 protein, human)
RN  - 0 (Tnfrsf11a protein, mouse)
RN  - 0 (Tnfsf11 protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/*metabolism
MH  - Cell Differentiation/physiology
MH  - Humans
MH  - Interleukin-1/*metabolism
MH  - Membrane Glycoproteins/*metabolism
MH  - Mice
MH  - Osteoclasts/cytology/*metabolism
MH  - RANK Ligand
MH  - Receptor Activator of Nuclear Factor-kappa B
MH  - Tumor Necrosis Factor-alpha/*metabolism
MH  - Up-Regulation
EDAT- 2004/05/12 05:00
MHDA- 2004/12/31 09:00
CRDT- 2004/05/12 05:00
PHST- 2004/02/02 00:00 [received]
PHST- 2004/02/15 00:00 [accepted]
PHST- 2004/05/12 05:00 [pubmed]
PHST- 2004/12/31 09:00 [medline]
PHST- 2004/05/12 05:00 [entrez]
AID - S1043466604000602 [pii]
AID - 10.1016/j.cyto.2004.02.001 [doi]
PST - ppublish
SO  - Cytokine. 2004 May 7;26(3):138-44. doi: 10.1016/j.cyto.2004.02.001.