PMID- 15678621
OWN - NLM
STAT- MEDLINE
DCOM- 20060831
LR  - 20191210
IS  - 1358-863X (Print)
IS  - 1358-863X (Linking)
VI  - 9
IP  - 4
DP  - 2004 Nov
TI  - Abnormal monocyte recruitment and collateral artery formation in monocyte 
      chemoattractant protein-1 deficient mice.
PG  - 287-92
AB  - Monocyte chemoattractant protein 1 (MCP-1) has been shown to be effective for the 
      stimulation of collateral artery formation in small and large animal models. The 
      availability of a genetic knockout mouse enables evaluation of the importance of 
      the role of MCP-1 in the natural course of collateral artery growth. In a total 
      of 21 MCP-1 -/- as well as 13 of the appropriate genetic background controls 
      ([129Sv/J X C57BI/6J]F1), a femoral artery ligation was performed. Subsequently, 
      a polyethylene catheter, connected to an osmotic minipump, was inserted 
      retrogradely into the occluded femoral artery with the tip pointing upstream. 
      Using this technique, PBS (MCP-1 -/-: n = 13 and C57BI/6J: n = 13) or MCP-1 (JE; 
      MCP-1 -/-: n = 8) was delivered intra-arterially. Seven days after ligation, 
      determination of hind limb flow was assessed by controlled tissue perfusion using 
      differently labeled fluorescent microspheres. MCP-1 -/- mice exhibited a 
      reduction of hind limb flow of 32.9 +/- 9.2% of the unligated hind limb, compared 
      with 55.4 +/- 6.8% in C57BI/6J mice (p<0.01). MCP-1 -/- mice that underwent a 
      subsequent 'rescue' treatment with MCP-1 showed a restoration of flow to a level 
      of 47.4 +/- 9.8% (p = NS compared with PBS-treated C57BI/6J). Specific 
      immunohistochemical staining for monocytes (MOMA-2: MCP-1 -/-, n = 5 and 
      C57BI/6J, n = 5) showed a reduced number of monocytes around developing 
      collateral arteries in the MCP-1 -/- mice. In conclusion, our data show that the 
      absence of MCP-1 causes a strong reduction in flow restoration after femoral 
      artery occlusion, coinciding with a reduced monocyte attraction, emphasizing the 
      central role of this chemokine in the multifactorial process of collateral artery 
      formation.
FAU - Voskuil, Michiel
AU  - Voskuil M
AD  - Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands.
FAU - Hoefer, Imo E
AU  - Hoefer IE
FAU - van Royen, Niels
AU  - van Royen N
FAU - Hua, Jing
AU  - Hua J
FAU - de Graaf, Stijn
AU  - de Graaf S
FAU - Bode, Christoph
AU  - Bode C
FAU - Buschmann, Ivo R
AU  - Buschmann IR
FAU - Piek, Jan J
AU  - Piek JJ
LA  - eng
PT  - Comparative Study
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Vasc Med
JT  - Vascular medicine (London, England)
JID - 9610930
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/*deficiency
MH  - *Collateral Circulation
MH  - Disease Models, Animal
MH  - Endothelium, Vascular/cytology/metabolism/physiopathology
MH  - Extremities/*blood supply/surgery
MH  - Female
MH  - Femoral Artery/cytology/metabolism/physiopathology
MH  - Immunohistochemistry
MH  - Ligation
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Monocytes/*metabolism/*pathology
MH  - Perfusion
MH  - Regional Blood Flow
EDAT- 2005/02/01 09:00
MHDA- 2006/09/01 09:00
CRDT- 2005/02/01 09:00
PHST- 2005/02/01 09:00 [pubmed]
PHST- 2006/09/01 09:00 [medline]
PHST- 2005/02/01 09:00 [entrez]
AID - 10.1191/1358863x04vm571oa [doi]
PST - ppublish
SO  - Vasc Med. 2004 Nov;9(4):287-92. doi: 10.1191/1358863x04vm571oa.