PMID- 12388329
OWN - NLM
STAT- MEDLINE
DCOM- 20021220
LR  - 20220316
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 283
IP  - 6
DP  - 2002 Dec
TI  - Role of endothelial MCP-1 in monocyte adhesion to inflamed human endothelium 
      under physiological flow.
PG  - H2584-91
AB  - Monocyte chemoattractant protein-1 (MCP-1) is an essential chemokine involved in 
      monocyte traffic across endo- and epithelial barriers both in vitro and in vivo. 
      However, the contribution of endothelial MCP-1 signaling via its CCR2 receptor in 
      monocyte adhesion to inflamed endothelium under flow is incompletely understood. 
      A sensitive flow chamber assay was used to assess monocyte adhesion to 
      TNF-alpha-activated primary human pulmonary artery endothelial cells (HPAEC) 
      during physiological shear stress. Monocyte adhesion was markedly reduced ( 
      approximately 45%) when HPAEC-derived MCP-1 was either neutralized with 
      anti-MCP-1 mAb or inhibited by translational arrest of MCP-1 mRNA transcripts 
      with MCP-1 antisense oligomers. Corresponding efficacy was observed for blockade 
      of monocyte CCR2 receptor function by anti-CCR2 mAb or MCP-1 antagonists (9-76 
      analog). The impact of endothelial MCP-1 on monocyte-HPAEC adhesion occurred via 
      beta(2)-integrin but not via beta(1)-integrin adhesion pathways. In this line, 
      pretreatment of monocytes with MCP-1 but not RANTES provoked a rapid and 
      transient neoepitope 24 expression on beta(2)-integrin alpha-chains, as analyzed 
      by increased reporter mAb24 binding. Collectively, our data show an important 
      cross talk of endothelial MCP-1 with monocyte CCR2 effecting monocyte firm 
      adhesion to inflamed HPAEC under physiological flow conditions.
FAU - Maus, U
AU  - Maus U
AD  - Department of Internal Medicine, Justus-Liebig University, Giessen 35392, 
      Germany. Ulrich.A.Maus@med.uni-giessen.de
FAU - Henning, S
AU  - Henning S
FAU - Wenschuh, H
AU  - Wenschuh H
FAU - Mayer, K
AU  - Mayer K
FAU - Seeger, W
AU  - Seeger W
FAU - Lohmeyer, J
AU  - Lohmeyer J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20020829
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (CCR2 protein, human)
RN  - 0 (CD18 Antigens)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Integrin beta1)
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (monocyte chemoattractant protein 1 (9-76))
SB  - IM
MH  - Antibodies, Monoclonal/pharmacology
MH  - CD18 Antigens/metabolism
MH  - Cell Adhesion/drug effects/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/antagonists & inhibitors/genetics/pharmacology/*physiology
MH  - Endothelium, Vascular/cytology/*physiopathology
MH  - Flow Cytometry
MH  - Hemorheology/methods
MH  - Humans
MH  - Inflammation/*physiopathology
MH  - Integrin beta1/metabolism
MH  - Monocytes/cytology/*physiology
MH  - Oligonucleotides, Antisense/pharmacology
MH  - Peptide Fragments/pharmacology
MH  - Pulmonary Artery/cytology
MH  - Receptor Cross-Talk/drug effects
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/antagonists & inhibitors/metabolism
EDAT- 2002/10/22 04:00
MHDA- 2002/12/21 04:00
CRDT- 2002/10/22 04:00
PHST- 2002/10/22 04:00 [pubmed]
PHST- 2002/12/21 04:00 [medline]
PHST- 2002/10/22 04:00 [entrez]
AID - 00349.2002 [pii]
AID - 10.1152/ajpheart.00349.2002 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2002 Dec;283(6):H2584-91. doi: 
      10.1152/ajpheart.00349.2002. Epub 2002 Aug 29.