PMID- 15059933
OWN - NLM
STAT- MEDLINE
DCOM- 20041007
LR  - 20061115
IS  - 1524-4571 (Electronic)
IS  - 0009-7330 (Linking)
VI  - 94
IP  - 9
DP  - 2004 May 14
TI  - Arteriogenesis proceeds via ICAM-1/Mac-1- mediated mechanisms.
PG  - 1179-85
AB  - Monocyte adhesion to shear stress-activated endothelium stands as an important 
      initial step during arteriogenesis (collateral artery growth). Using multiple 
      approaches, we tested the hypothesis that monocyte adhesion via intercellular 
      adhesion molecule-1 (ICAM-1) and selectin interactions is essential for adaptive 
      arteriogenesis. Forty-eight New Zealand White rabbits received either solvent, 
      monocyte chemoattractant protein-1 (MCP-1) alone, MCP-1 plus ICAM-mab, or MCP-1 
      plus an IgG2a isotype control via osmotic minipumps. After 7 days, collateral 
      conductance was evaluated: solvent 4.01 (mL/min per 100 mm Hg), MCP-1 plus 
      ICAM-mab 8.04 (versus solvent P=NS), and MCP-1 alone 33.11 (versus solvent 
      P<0.05). Furthermore, the right femoral arteries of ICAM-1-/-, Mac-1-/- and mice 
      having defective selectin interactions (FT4/7-/-) as well as their corresponding 
      controls were ligated. One week later, perfusion ratios were determined by the 
      use of fluorescent microspheres. FT4/7-/- mice did not show any significant 
      difference in perfusion restoration whereas ICAM-1-/- and Mac-1-/- mice had a 
      significant reduction in arteriogenesis as compared with matching controls 
      (FT4/7-WT 37+/-9%, FT4/7-/- 32+/-3%, P=0.31; C57BL/6J 59+/-9%, ICAM-1-/- 36+/-8%, 
      P<0.05; Mac-1-/- 42+/-3%, P<0.05). ICAM-1/Mac-1-mediated monocyte adhesion to the 
      endothelium of collateral arteries is an essential step for arteriogenesis, 
      whereas this process can proceed via selectin interaction independent mechanisms. 
      Furthermore, in vivo treatment with monoclonal antibodies against ICAM-1 totally 
      abolishes the stimulatory effect of MCP-1 on collateral artery growth, suggesting 
      that the mechanism of the MCP-1-induced arteriogenesis proceeds via the 
      localization of monocytes rather than the action of the MCP-1 molecule itself.
FAU - Hoefer, Imo E
AU  - Hoefer IE
AD  - Research Group for Experimental and Clinical Arteriogenesis at the Department of 
      Cardiology, University of Freiburg, Freiburg, Germany. 
      hoefer@med1.ukl.uni-freiburg.de
FAU - van Royen, Niels
AU  - van Royen N
FAU - Rectenwald, John E
AU  - Rectenwald JE
FAU - Deindl, Elisabeth
AU  - Deindl E
FAU - Hua, Jing
AU  - Hua J
FAU - Jost, Marco
AU  - Jost M
FAU - Grundmann, Sebastian
AU  - Grundmann S
FAU - Voskuil, Michiel
AU  - Voskuil M
FAU - Ozaki, C Keith
AU  - Ozaki CK
FAU - Piek, Jan J
AU  - Piek JJ
FAU - Buschmann, Ivo R
AU  - Buschmann IR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20040401
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Macrophage-1 Antigen)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Cell Adhesion
MH  - Chemokine CCL2/*pharmacology
MH  - Endothelial Cells/cytology/drug effects/metabolism
MH  - Endothelium, Vascular/*cytology
MH  - Immunoglobulin G/pharmacology
MH  - Intercellular Adhesion Molecule-1/genetics/immunology/*physiology
MH  - Macrophage-1 Antigen/genetics/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Microspheres
MH  - Monocytes/*cytology/drug effects/metabolism
MH  - Neovascularization, Physiologic/drug effects/genetics/*physiology
MH  - Rabbits
MH  - Random Allocation
EDAT- 2004/04/03 05:00
MHDA- 2004/10/08 09:00
CRDT- 2004/04/03 05:00
PHST- 2004/04/03 05:00 [pubmed]
PHST- 2004/10/08 09:00 [medline]
PHST- 2004/04/03 05:00 [entrez]
AID - 01.RES.0000126922.18222.F0 [pii]
AID - 10.1161/01.RES.0000126922.18222.F0 [doi]
PST - ppublish
SO  - Circ Res. 2004 May 14;94(9):1179-85. doi: 10.1161/01.RES.0000126922.18222.F0. 
      Epub 2004 Apr 1.