PMID- 7622526
OWN - NLM
STAT- MEDLINE
DCOM- 19950825
LR  - 20210210
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 270
IP  - 28
DP  - 1995 Jul 14
TI  - Nitric oxide inhibits macrophage-colony stimulating factor gene transcription in 
      vascular endothelial cells.
PG  - 17050-5
AB  - Macrophage-colony stimulating factor (M-CSF) contributes to atherogenesis by 
      regulating macrophage-derived foam cells in atherosclerotic lesions. Here we 
      report that nitric oxide (NO) inhibits the expression of M-CSF in human vascular 
      endothelial cells independent of guanylyl cyclase activation. The induction of 
      M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or 
      tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, 
      S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 
      3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. 
      Inhibition of endogenous NO production by N-monomethyl-L-arginine (L-NMA) also 
      increased M-CSF expression in control and TNF alpha-stimulated cells. Nuclear 
      run-on assays and transfection studies using M-CSF promoter constructs linked to 
      chloramphenicol acetyltransferase reporter gene indicated that NO repressed M-CSF 
      gene transcription through nuclear factor-kappa B (NF-kappa B). Electrophoretic 
      mobility shift assays demonstrated that activation of NF-kappa B by L-NMA, 
      ox-LDL, and TNF alpha was attenuated by GSNO and SNP, but not by glutathione or 
      cGMP analogues. Since the induction of M-CSF expression depends upon NF-kappa B 
      activation, the ability of NO to inhibit NF-kappa B activation and M-CSF 
      expression may contribute to some of NO's antiatherogenic properties.
FAU - Peng, H B
AU  - Peng HB
AD  - Cardiovascular Division, Brigham & Women's Hospital, Boston, Massachusetts, USA.
FAU - Rajavashisth, T B
AU  - Rajavashisth TB
FAU - Libby, P
AU  - Libby P
FAU - Liao, J K
AU  - Liao JK
LA  - eng
GR  - HL02508/HL/NHLBI NIH HHS/United States
GR  - HL34636/HL/NHLBI NIH HHS/United States
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 Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitroso Compounds)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 57564-91-7 (S-Nitrosoglutathione)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*metabolism
MH  - *Gene Expression Regulation
MH  - Glutathione/analogs & derivatives/pharmacology
MH  - Humans
MH  - Lipoproteins, LDL/pharmacology
MH  - Macrophage Colony-Stimulating Factor/*genetics
MH  - Molecular Sequence Data
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide/*physiology
MH  - Nitroso Compounds/pharmacology
MH  - S-Nitrosoglutathione
MH  - Transcription, Genetic/drug effects
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1995/07/14 00:00
MHDA- 1995/07/14 00:01
CRDT- 1995/07/14 00:00
PHST- 1995/07/14 00:00 [pubmed]
PHST- 1995/07/14 00:01 [medline]
PHST- 1995/07/14 00:00 [entrez]
AID - S0021-9258(17)46947-X [pii]
AID - 10.1074/jbc.270.28.17050 [doi]
PST - ppublish
SO  - J Biol Chem. 1995 Jul 14;270(28):17050-5. doi: 10.1074/jbc.270.28.17050.