PMID- 8647916
OWN - NLM
STAT- MEDLINE
DCOM- 19960725
LR  - 20131121
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 168
IP  - 1
DP  - 1996 Jul
TI  - Tumor necrosis factor-alpha induces transcription of the colony-stimulating 
      factor-1 gene in murine osteoblasts.
PG  - 199-208
AB  - Tumor necrosis factor-alpha (TNF-alpha) stimulates bone resorption both in vitro 
      and in vivo. The cellular mechanisms for this effect are not known but one 
      pathway may be via release of osteoblast derived factors which stimulate 
      osteoclast formation. Because colony-stimulating factor-1 (CSF-1) is essential 
      for osteoclast progenitor proliferation, we examined the effect of TNF-alpha on 
      osteoblast expression of CSF-1. TNF-alpha treatment of MC3T3-E1 or primary mouse 
      osteoblasts stimulated the secretion of an activity that was mitogenic for a 
      CSF-1 responsive cell line and was completely neutralized by antiserum to CSF-1. 
      By Northern analysis, TNF-alpha caused a dose and time (3 to 24 h) dependent 
      increase in CSF-1 transcript expression in MC3T3-E1 cells. mRNA stability studies 
      using actinomycin D revealed that TNF-alpha does not affect CSF-1 mRNA half-life 
      in MC3T3-E1 cells, while nuclear-run off analysis demonstrated that TNF-alpha 
      increases CSF-1 gene transcription. Cycloheximide treatment of MC3T3-E1 cells 
      up-regulated CSF-1 mRNA, and compared to either agent alone, cycloheximide and 
      TNF-alpha in combination resulted in augmentation of CSF-1 expression. A series 
      of studies using both agonists and inhibitors indicated that TNF-alpha-induced 
      CSF-1 expression did not involve the arachidonic acid, PKC, or cAMP pathways. 
      These results suggest that TNF-alpha induces CSF-1 expression in osteoblasts by a 
      transcriptional mechanism which is largely independent of new protein synthesis 
      and of the second messenger pathways examined.
FAU - Kaplan, D L
AU  - Kaplan DL
AD  - Section of Comparative Medicine, Yale University School of Medicine, New Haven, 
      Connecticut 06520, USA.
FAU - Eielson, C M
AU  - Eielson CM
FAU - Horowitz, M C
AU  - Horowitz MC
FAU - Insogna, K L
AU  - Insogna KL
FAU - Weir, E C
AU  - Weir EC
LA  - eng
GR  - AR39571/AR/NIAMS NIH HHS/United States
GR  - AR40507/AR/NIAMS NIH HHS/United States
GR  - DK45228/DK/NIDDK NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1F7A44V6OU (Colforsin)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.11.13 (Protein Kinase C)
SB  - IM
MH  - Animals
MH  - Bone Resorption
MH  - Cells, Cultured
MH  - Colforsin/pharmacology
MH  - Cyclic AMP/metabolism/physiology
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression
MH  - Macrophage Colony-Stimulating Factor/*genetics
MH  - Mice
MH  - Osteoblasts/*metabolism
MH  - Protein Kinase C/physiology
MH  - RNA, Messenger/genetics
MH  - Second Messenger Systems
MH  - Transcription, Genetic/*drug effects
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1996/07/01 00:00
MHDA- 2000/06/20 09:00
CRDT- 1996/07/01 00:00
PHST- 1996/07/01 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1996/07/01 00:00 [entrez]
AID - 10.1002/(SICI)1097-4652(199607)168:1<199::AID-JCP24>3.0.CO;2-1 [pii]
AID - 10.1002/(SICI)1097-4652(199607)168:1<199::AID-JCP24>3.0.CO;2-1 [doi]
PST - ppublish
SO  - J Cell Physiol. 1996 Jul;168(1):199-208. doi: 
      10.1002/(SICI)1097-4652(199607)168:1<199::AID-JCP24>3.0.CO;2-1.