PMID- 10982549
OWN - NLM
STAT- MEDLINE
DCOM- 20000928
LR  - 20220227
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 102
IP  - 11
DP  - 2000 Sep 12
TI  - Monocyte chemoattractant protein-1 is upregulated in rats with volume-overload 
      congestive heart failure.
PG  - 1315-22
AB  - BACKGROUND: Chemokines are potent proinflammatory and immune modulators. 
      Increased expression of chemokines, eg, monocyte chemoattractant protein-1 
      (MCP-1), has recently been described in clinical and experimental heart failure. 
      The present report is aimed at exploring the expression, localization, and 
      binding site regulation of MCP-1, a member of the C-C chemokine family, in a rat 
      model of volume-overload congestive heart failure (CHF). METHODS AND RESULTS: An 
      aortocaval fistula was surgically created between the abdominal aorta and 
      inferior vena cava. Rats with CHF were further subdivided into compensated and 
      decompensated subgroups. Northern blot analysis and real-time quantitative 
      polymerase chain reaction demonstrated upregulation of MCP-1 mRNA expression 
      correlating with the severity of CHF (288+/-22, 502+/-62, and 826+/-138 copies/ng 
      total RNA for sham, compensated, and decompensated animals, respectively; n=5, 
      P:<0.05). MCP-1 protein was localized by immunohistochemistry in cardiomyocytes, 
      vascular endothelium and smooth muscle cells, infiltrating leukocytes, and 
      interstitial fibroblasts, and its intensity increased with severity of CHF. In 
      addition, rats with CHF displayed a significant decrease of (125)I-labeled MCP-1 
      binding sites to myocardium-derived membranes (384.3+/-57.0, 181.3+/-8.8, and 
      123.3+/-14.1 fmol/mg protein for sham, compensated, and decompensated animals, 
      respectively). CONCLUSIONS: Volume-overload CHF in rats is associated with 
      alterations in the expression, immunohistochemical localization, and receptor 
      binding of the MCP-1 chemokine in the myocardium. These changes were more 
      pronounced in rats with decompensated CHF. The data suggest that activation of 
      the MCP-1 system may contribute to the progressive cardiac decompensation and 
      development of CHF in rats with aortocaval fistula.
FAU - Behr, T M
AU  - Behr TM
AD  - Cardiovascular Pharmacology, SmithKline Beecham, King of Prussia, PA 19406, USA. 
      thomas_m_behr@sbphrd.com
FAU - Wang, X
AU  - Wang X
FAU - Aiyar, N
AU  - Aiyar N
FAU - Coatney, R W
AU  - Coatney RW
FAU - Li, X
AU  - Li X
FAU - Koster, P
AU  - Koster P
FAU - Angermann, C E
AU  - Angermann CE
FAU - Ohlstein, E
AU  - Ohlstein E
FAU - Feuerstein, G Z
AU  - Feuerstein GZ
FAU - Winaver, J
AU  - Winaver J
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Binding, Competitive
MH  - Blotting, Northern
MH  - Chemokine CCL2/*metabolism
MH  - Heart Failure/diagnostic imaging/*metabolism
MH  - Immunohistochemistry
MH  - In Vitro Techniques
MH  - Male
MH  - Myocardium/metabolism
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/metabolism
MH  - Radioligand Assay
MH  - Rats
MH  - Rats, Wistar
MH  - Ultrasonography
MH  - Up-Regulation
EDAT- 2000/09/12 00:00
MHDA- 2000/09/30 00:00
CRDT- 2000/09/12 00:00
PHST- 2000/09/12 00:00 [pubmed]
PHST- 2000/09/30 00:00 [medline]
PHST- 2000/09/12 00:00 [entrez]
AID - 10.1161/01.cir.102.11.1315 [doi]
PST - ppublish
SO  - Circulation. 2000 Sep 12;102(11):1315-22. doi: 10.1161/01.cir.102.11.1315.