PMID- 16039282
OWN - NLM
STAT- MEDLINE
DCOM- 20051207
LR  - 20061115
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 181
IP  - 2
DP  - 2005 Aug
TI  - Leukocyte subpopulations and arteriogenesis: specific role of monocytes, 
      lymphocytes and granulocytes.
PG  - 285-93
AB  - OBJECTIVE: Circulating leukocytes play a crucial role during arteriogenesis. 
      However, known pro-arteriogenic compounds (MCP-1, GM-CSF) acting via monocytic 
      pathways also exert positive effects on granulocytes and lymphocytes. The role of 
      these two cell types in arteriogenesis remains yet to be clarified, which was the 
      aim of the current study. METHODS: Ninety New Zealand White Rabbits received 
      either phosphate buffered saline (PBS), monocyte chemoattractant protein-1 
      (MCP-1), interleukin-8 (IL-8), neutrophil activating protein-2 (NAP-2) or 
      lymphotactin (Ltn) via osmotic minipumps after unilateral femoral artery 
      ligation. In vitro stimulation and in vivo assessment of chemoattraction 
      confirmed cell-specific action of the compounds in rabbits. Arteriogenesis was 
      evaluated by angiography and collateral conductance measurements using 
      fluorescent microspheres. Quantitative immunohistology was used to quantify 
      transmigrated leukocyte subtypes after infusion of the factors. RESULTS: MCP-1 
      infusion attracts monocytes and granulocytes, whereas IL-8 attracts all three 
      cell types albeit monocytes to a significantly lower degree than MCP-1. NAP-2 and 
      lymphotactin selectively attract granulocytes, respectively, lymphocytes. Of the 
      tested cytokines, only MCP-1 stimulates arteriogenesis, as assessed by collateral 
      conductance measurements ((ml/(min 100 mmHg)): PBS, 50.70+/-5.15; MCP-1, 
      216.30+/-12.30; IL-8, 58.91+/-5.56; NAP-2, 66.83+/-8.72; Ltn, 52.80+/-5.37) and 
      angiographic findings. CONCLUSION: This study for the first time provides 
      evidence that not granulocytes or T-lymphocytes but monocytes are the key 
      mediators of arteriogenesis.
FAU - Hoefer, Imo E
AU  - Hoefer IE
AD  - Research Group for Experimental and Clinical Arteriogenesis, Department of 
      Cardiology, University of Freiburg, Germany. i.hoefer@azu.nl
FAU - Grundmann, Sebastian
AU  - Grundmann S
FAU - van Royen, Niels
AU  - van Royen N
FAU - Voskuil, Michiel
AU  - Voskuil M
FAU - Schirmer, Stephan H
AU  - Schirmer SH
FAU - Ulusans, Susann
AU  - Ulusans S
FAU - Bode, Christoph
AU  - Bode C
FAU - Buschmann, Ivo R
AU  - Buschmann IR
FAU - Piek, Jan J
AU  - Piek JJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Lymphokines)
RN  - 0 (PPBP protein, human)
RN  - 0 (Peptides)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (beta-Thromboglobulin)
RN  - 0 (lymphotactin)
SB  - IM
MH  - Animals
MH  - Arteries/immunology
MH  - Chemokine CCL2/pharmacology
MH  - Chemotaxis, Leukocyte/drug effects
MH  - Collateral Circulation/drug effects/*immunology
MH  - Granulocytes/physiology
MH  - Interleukin-8/pharmacology
MH  - Leukocytes/*physiology
MH  - Lymphocytes/physiology
MH  - Lymphokines/pharmacology
MH  - Monocytes/physiology
MH  - Neovascularization, Physiologic/drug effects/*immunology
MH  - Peptides/pharmacology
MH  - Rabbits
MH  - Sialoglycoproteins/pharmacology
MH  - beta-Thromboglobulin
EDAT- 2005/07/26 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/07/26 09:00
PHST- 2004/11/25 00:00 [received]
PHST- 2005/01/21 00:00 [revised]
PHST- 2005/01/27 00:00 [accepted]
PHST- 2005/07/26 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/07/26 09:00 [entrez]
AID - S0021-9150(05)00103-6 [pii]
AID - 10.1016/j.atherosclerosis.2005.01.047 [doi]
PST - ppublish
SO  - Atherosclerosis. 2005 Aug;181(2):285-93. doi: 
      10.1016/j.atherosclerosis.2005.01.047.