PMID- 18753699
OWN - NLM
STAT- MEDLINE
DCOM- 20081231
LR  - 20211203
IS  - 1346-9843 (Print)
IS  - 1346-9843 (Linking)
VI  - 72
IP  - 10
DP  - 2008 Oct
TI  - Angiotensin-receptor blockade reduces border zone myocardial monocyte 
      chemoattractant protein-1 expression and macrophage infiltration in 
      post-infarction ventricular remodeling.
PG  - 1685-92
AB  - BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is a key mediator of left 
      ventricular (LV) remodeling during the early phase of myocardial infarction (MI). 
      The hypothesis tested was that myocardial MCP-1 expression would increase during 
      the chronic phase of MI and an angiotensin-II type 1 receptor blocker (ARB) would 
      attenuate macrophage infiltration through decreased myocardial MCP-1 expression. 
      METHODS AND RESULTS: MI was produced by ligation of the left coronary artery in 
      Wistar rats, which were then randomized to treatment with vehicle (MI/C), 
      candesartan (10 mg.kg(-1).day(-1)) for 6 weeks (MI/ARB0-6W), or candesartan for 2 
      weeks, starting 4 weeks after MI (MI/ARB4-6W). LV systolic and end-diastolic 
      pressures 6 weeks after MI were decreased in MI/ARB0-6W compared with MI/C or 
      MI/ARB4-6W, however, there were no differences in other hemodynamic or 
      echocardiographic parameters among infarcted rat groups. Both long- and 
      short-term treatments with ARB similarly reduced mRNA expressions of MCP-1, 
      transforming growth factor-beta1, and procollagen type I and III, macrophage 
      infiltration, and myocardial fibrosis in the border zone. CONCLUSIONS: In post-MI 
      heart failure, ARB attenuated MCP-1 expression and macrophage infiltration in the 
      border zone, resulting in less myocardial fibrosis. ARB may exert its beneficial 
      effect, at least in part, by inhibiting myocardial macrophage-related 
      inflammation.
FAU - Kohno, Takashi
AU  - Kohno T
AD  - Division of Cardiology, Department of Medicine, Keio University School of 
      Medicine, Tokyo, Japan.
FAU - Anzai, Toshihisa
AU  - Anzai T
FAU - Naito, Kotaro
AU  - Naito K
FAU - Sugano, Yasuo
AU  - Sugano Y
FAU - Maekawa, Yuichiro
AU  - Maekawa Y
FAU - Takahashi, Toshiyuki
AU  - Takahashi T
FAU - Yoshikawa, Tsutomu
AU  - Yoshikawa T
FAU - Ogawa, Satoshi
AU  - Ogawa S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080828
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Benzimidazoles)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA Primers)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tetrazoles)
RN  - 63231-63-0 (RNA)
RN  - 9007-34-5 (Collagen)
RN  - S8Q36MD2XX (candesartan)
SB  - IM
MH  - Angiotensin II Type 1 Receptor Blockers/*therapeutic use
MH  - *Angiotensin Receptor Antagonists
MH  - Animals
MH  - Benzimidazoles/*therapeutic use
MH  - Biphenyl Compounds
MH  - Chemokine CCL2/*genetics
MH  - Collagen/metabolism
MH  - DNA Primers
MH  - Disease Models, Animal
MH  - Male
MH  - Myocardial Infarction/*pathology/prevention & control
MH  - RNA/genetics
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tetrazoles/*therapeutic use
MH  - Ventricular Remodeling/drug effects/*physiology
EDAT- 2008/08/30 09:00
MHDA- 2009/01/01 09:00
CRDT- 2008/08/30 09:00
PHST- 2008/08/30 09:00 [pubmed]
PHST- 2009/01/01 09:00 [medline]
PHST- 2008/08/30 09:00 [entrez]
AID - JST.JSTAGE/circj/CJ-08-0115 [pii]
AID - 10.1253/circj.cj-08-0115 [doi]
PST - ppublish
SO  - Circ J. 2008 Oct;72(10):1685-92. doi: 10.1253/circj.cj-08-0115. Epub 2008 Aug 28.