PMID- 15470479
OWN - NLM
STAT- MEDLINE
DCOM- 20050203
LR  - 20121115
IS  - 0969-7128 (Print)
IS  - 0969-7128 (Linking)
VI  - 11
IP  - 23
DP  - 2004 Dec
TI  - Nonviral monocyte chemoattractant protein-1 gene transfer improves arteriogenesis 
      after femoral artery occlusion.
PG  - 1685-93
AB  - Local infusion of recombinant monocyte chemoattractant protein-1 (MCP-1) has been 
      shown to enhance collateral artery formation in rabbit and pig hindlimb models. 
      Owing to clinical disadvantages of protein infusion, a nonviral, liposome-based 
      MCP-1 gene transfer was developed. Collateralization in a porcine hindlimb model 
      served to provide a proof-of-principle for the functional benefit of MCP-1 
      overexpression. Development of arterial conductance as a measure of functionally 
      relevant collateralization was evaluated in occluded as well as untreated 
      hindlimbs in each animal. At the time of occlusion, MCP-1 and control DNA/DC-30 
      lipoplexes were transferred to femoral arteries of Goettingen minipigs (two 
      therapeutic MCP-1 groups: 2 and 4 microg and one control group), using the 
      Infiltrator local drug-delivery device. At 2 weeks following occlusion, 
      collateralization was determined as changes in peripheral haemodynamic 
      conductance, peripheral over aortic blood pressure ratio and angiographically 
      visible morphology of the peripheral vessel tree. Nonviral MCP-1 gene transfer 
      significantly improved peripheral conductance (control 11.69+/-2.78%, 2 microg 
      23.81+/-2.81%, P<0.05 and 4 microg 23.36+/-3.1%, P<0.05; n=12 per group) as well 
      as the ratio of peripheral over aortic blood pressure (control 0.64+/-0.03%, 2 
      microg 0.75+/-0.02%, P<0.05 and 4 mug 0.75+/-0.02%, P<0.05; n=12 per group) when 
      compared to the untreated controls 2 weeks after occlusion. Thus, it could be 
      demonstrated for the first time that in situ overexpression of MCP-1 following 
      local nonviral gene transfer is a potential approach to improve peripheral 
      collateralization.
FAU - Muhs, A
AU  - Muhs A
AD  - Cardion AG, Erkrath, Germany.
FAU - Lenter, M C
AU  - Lenter MC
FAU - Seidler, R W
AU  - Seidler RW
FAU - Zweigerdt, R
AU  - Zweigerdt R
FAU - Kirchengast, M
AU  - Kirchengast M
FAU - Weser, R
AU  - Weser R
FAU - Ruediger, M
AU  - Ruediger M
FAU - Guth, Brian
AU  - Guth B
LA  - eng
PT  - Journal Article
PL  - England
TA  - Gene Ther
JT  - Gene therapy
JID - 9421525
RN  - 0 (Chemokine CCL2)
RN  - 0 (Liposomes)
SB  - IM
MH  - Animals
MH  - Arterial Occlusive Diseases/metabolism/*therapy
MH  - Chemokine CCL2/*genetics/metabolism
MH  - Collateral Circulation/*genetics
MH  - Disease Models, Animal
MH  - *Femoral Artery/metabolism
MH  - Gene Expression
MH  - Genetic Therapy/*methods
MH  - Liposomes
MH  - Peripheral Vascular Diseases/metabolism/*therapy
MH  - Plasmids
MH  - Polymerase Chain Reaction/methods
MH  - Swine
MH  - Swine, Miniature
MH  - Transfection
MH  - Transgenes
EDAT- 2004/10/08 09:00
MHDA- 2005/02/04 09:00
CRDT- 2004/10/08 09:00
PHST- 2004/10/08 09:00 [pubmed]
PHST- 2005/02/04 09:00 [medline]
PHST- 2004/10/08 09:00 [entrez]
AID - 3302360 [pii]
AID - 10.1038/sj.gt.3302360 [doi]
PST - ppublish
SO  - Gene Ther. 2004 Dec;11(23):1685-93. doi: 10.1038/sj.gt.3302360.