PMID- 12223446
OWN - NLM
STAT- MEDLINE
DCOM- 20021216
LR  - 20121115
IS  - 1530-6860 (Electronic)
IS  - 0892-6638 (Linking)
VI  - 16
IP  - 13
DP  - 2002 Nov
TI  - Anti-monocyte chemoattractant protein-1 gene therapy inhibits restenotic changes 
      (neointimal hyperplasia) after balloon injury in rats and monkeys.
PG  - 1838-40
AB  - Prevention of restenosis after coronary intervention is a major clinical 
      challenge, which highlights the need of new therapeutic options. Vascular injury 
      may involve inflammatory responses that accelerate the recruitment and activation 
      of monocytes through the activation of chemotactic factors, including monocyte 
      chemoattractant protein-1 (MCP-1). However, there is no definitive evidence 
      supporting the role of MCP-1 in restenosis. We recently devised a new strategy 
      for anti-MCP-1 gene therapy by transfecting an N-terminal deletion mutant of the 
      MCP-1 gene into skeletal muscles. We demonstrate here that this strategy 
      suppressed monocyte infiltration/activation in the injured site and markedly 
      inhibited restenotic changes (neointimal hyperplasia) after balloon injury of the 
      carotid artery in rats and monkeys. This strategy also suppressed the local 
      production of MCP-1 and inflammatory cytokines. Therefore, monocyte infiltration 
      and activation mediated by MCP-1 are essential in the development of restenotic 
      changes after balloon injury. This strategy may be a useful form of gene therapy 
      against human restenosis.
FAU - Usui, Makoto
AU  - Usui M
AD  - Department of Cardiovascular Medicine, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Egashira, Kensuke
AU  - Egashira K
FAU - Ohtani, Kisho
AU  - Ohtani K
FAU - Kataoka, Chu
AU  - Kataoka C
FAU - Ishibashi, Minako
AU  - Ishibashi M
FAU - Hiasa, Ken-ichi
AU  - Hiasa K
FAU - Katoh, Makoto
AU  - Katoh M
FAU - Zhao, Qingwei
AU  - Zhao Q
FAU - Kitamoto, Shiro
AU  - Kitamoto S
FAU - Takeshita, Akira
AU  - Takeshita A
LA  - eng
PT  - Journal Article
DEP - 20020905
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American Societies for 
      Experimental Biology
JID - 8804484
RN  - 0 (Actins)
RN  - 0 (CCR2 protein, human)
RN  - 0 (Ccr2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Proliferating Cell Nuclear Antigen)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (von Willebrand Factor)
SB  - IM
MH  - Actins/analysis
MH  - Animals
MH  - Carotid Arteries/metabolism/pathology
MH  - Carotid Artery Injuries/etiology/*prevention & control
MH  - Catheterization/adverse effects
MH  - Chemokine CCL2/blood/*genetics/metabolism
MH  - Chemokines/metabolism
MH  - Cytokines/metabolism
MH  - Hyperplasia
MH  - Immunohistochemistry
MH  - Macaca fascicularis
MH  - Male
MH  - Muscle, Smooth/chemistry
MH  - Mutation
MH  - Plasmids/genetics
MH  - Proliferating Cell Nuclear Antigen/analysis
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Inbred WKY
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/genetics/metabolism
MH  - Time Factors
MH  - Transfection
MH  - Tunica Intima/metabolism/*pathology
MH  - von Willebrand Factor/analysis
EDAT- 2002/09/12 10:00
MHDA- 2002/12/18 04:00
CRDT- 2002/09/12 10:00
PHST- 2002/09/12 10:00 [pubmed]
PHST- 2002/12/18 04:00 [medline]
PHST- 2002/09/12 10:00 [entrez]
AID - 02-0094fje [pii]
AID - 10.1096/fj.02-0094fje [doi]
PST - ppublish
SO  - FASEB J. 2002 Nov;16(13):1838-40. doi: 10.1096/fj.02-0094fje. Epub 2002 Sep 5.