PMID- 14527174
OWN - NLM
STAT- MEDLINE
DCOM- 20040426
LR  - 20190922
IS  - 0360-3997 (Print)
IS  - 0360-3997 (Linking)
VI  - 27
IP  - 4
DP  - 2003 Aug
TI  - Nitric oxide modulates MCP-1 expression in endothelial cells: implications for 
      the pathogenesis of pulmonary granulomatous vasculitis.
PG  - 213-23
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a pivotal mediator of angiocentric 
      granuloma formation in glucan-induced pulmonary granulomatous vasculitis. Based 
      on the rationale that mononuclear phagocytes retrieved from granulomas are rich 
      sources of nitric oxide (NO) and that the recruitment of mononuclear phagocytes 
      into lesions abates as granuloma formation slows, we tested the hypothesis that 
      MCP-1 gene expression is regulated by a NO-sensitive mechanism. Preexposure of 
      endothelial cell (EC) monolayers to NO donor compounds markedly reduced 
      cytokine-induced MCP-1 expression and cytosolic-to-nuclear translocation of 
      nuclear factor-kappa B (NF-kappaB), reversed fluctuations in endothelial reduced 
      glutathione (GSH) pools but did not affect cGMP concentrations. The lungs of mice 
      bearing targeted disruptions of the inducible nitric oxide synthase (iNOS) gene 
      exhibited significantly higher concentrations of MCP-1 following glucan infusion 
      than did those of wild-type mice. Cumulatively, these data suggest that NO 
      suppresses MCP-1 expression by blunting the redox changes associated with 
      cytokine-induced EC activation.
FAU - Desai, Anjali
AU  - Desai A
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor, 
      Michigan 48109-0602, USA.
FAU - Miller, Mark J
AU  - Miller MJ
FAU - Huang, Xiaodong
AU  - Huang X
FAU - Warren, Jeffrey S
AU  - Warren JS
LA  - eng
GR  - R01 HL 48287/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
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  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Chemokine CCL2)
RN  - 0 (Nitric Oxide Donors)
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/antagonists & inhibitors/*biosynthesis
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Endothelium, Vascular/drug effects/metabolism
MH  - Gene Expression Regulation/drug effects/physiology
MH  - Granuloma, Respiratory Tract/*metabolism
MH  - Humans
MH  - Mice
MH  - Mice, Knockout
MH  - Nitric Oxide/*physiology
MH  - Nitric Oxide Donors/pharmacology
MH  - Vasculitis/*metabolism
EDAT- 2003/10/07 05:00
MHDA- 2004/04/27 05:00
CRDT- 2003/10/07 05:00
PHST- 2003/10/07 05:00 [pubmed]
PHST- 2004/04/27 05:00 [medline]
PHST- 2003/10/07 05:00 [entrez]
AID - 10.1023/a:1025036530605 [doi]
PST - ppublish
SO  - Inflammation. 2003 Aug;27(4):213-23. doi: 10.1023/a:1025036530605.