PMID- 12426210
OWN - NLM
STAT- MEDLINE
DCOM- 20021204
LR  - 20190901
IS  - 1524-4636 (Electronic)
IS  - 1079-5642 (Linking)
VI  - 22
IP  - 11
DP  - 2002 Nov 1
TI  - Endothelial determinants of dendritic cell adhesion and migration: new 
      implications for vascular diseases.
PG  - 1817-23
AB  - OBJECTIVE: Atherosclerosis is a chronic disease triggered by endothelial injury 
      and sustained by inflammation. Dendritic cells (DCs) are critical for the 
      cell-mediated arm of an immune response and are known to influence inflammatory 
      immunity. A fundamental aspect of DC function is their capacity to adhere and 
      migrate through vascular endothelial cells (ECs). We investigated the role of 
      endothelial activation and dysregulation of the NO pathway on DC adhesion and 
      migration. METHODS AND RESULTS: We discovered that DC adhesion and migration are 
      modulated by changes in endothelial function. DC adhesion and transmigration were 
      markedly increased after exposing ECs to hypoxia, oxidized low density 
      lipoprotein, or tumor necrosis factor-alpha. Specifically, inhibition of 
      endothelial NO synthase increased DC binding and transmigration. L-Arginine or 
      3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition partially decreased 
      DC-EC interaction. CONCLUSIONS: The results of this study suggest that the 
      adhesion and migration of DCs are increased by stimuli known to accelerate 
      atherogenesis. Vice versa, augmentation of endothelial NO synthase activity 
      prevents DC adhesion. These findings may provide insight into the inflammatory 
      processes occurring in atherosclerosis. Because DCs control immunity, regulating 
      DC-EC interaction may be relevant to inflammation and atherogenesis.
FAU - Weis, Michael
AU  - Weis M
AD  - Division of Cardiovascular Medicine, Stanford University School of Medicine, 
      Stanford, Calif, USA. miweis@med.uni-muenchen.de
FAU - Schlichting, Christoph L
AU  - Schlichting CL
FAU - Engleman, Edgar G
AU  - Engleman EG
FAU - Cooke, John P
AU  - Cooke JP
LA  - eng
GR  - CA09151-26/CA/NCI NIH HHS/United States
GR  - R01 HL-58638/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  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (CD11c Antigen)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
SB  - IM
MH  - Aorta/cytology
MH  - Apoptosis/physiology
MH  - CD11c Antigen/biosynthesis
MH  - Cell Adhesion/physiology
MH  - Cell Adhesion Molecules/physiology
MH  - Cell Lineage
MH  - Cell Movement/*physiology
MH  - Cells, Cultured
MH  - Dendritic Cells/chemistry/metabolism/*physiology
MH  - Endothelium/*chemistry/metabolism/physiology
MH  - Endothelium, Vascular/cytology/metabolism/physiology
MH  - HLA-DR Antigens/biosynthesis
MH  - Humans
MH  - Lipopolysaccharide Receptors/biosynthesis
MH  - Nitric Oxide/metabolism/physiology
MH  - Nitric Oxide Synthase/metabolism
MH  - Nitric Oxide Synthase Type III
MH  - Oxygen Consumption/physiology
MH  - Skin/blood supply/cytology
MH  - Stem Cells/chemistry/metabolism/physiology
EDAT- 2002/11/12 04:00
MHDA- 2002/12/05 04:00
CRDT- 2002/11/12 04:00
PHST- 2002/11/12 04:00 [pubmed]
PHST- 2002/12/05 04:00 [medline]
PHST- 2002/11/12 04:00 [entrez]
AID - 10.1161/01.atv.0000036418.04998.d5 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 2002 Nov 1;22(11):1817-23. doi: 
      10.1161/01.atv.0000036418.04998.d5.