PMID- 11472393
OWN - NLM
STAT- MEDLINE
DCOM- 20010830
LR  - 20190513
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 124
IP  - 3
DP  - 2001 Jun
TI  - Enhanced expression and production of monocyte chemoattractant protein-1 in 
      myocarditis.
PG  - 346-52
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a member of the C-C chemokine 
      family that has been shown to play a major role in the migration of monocytes and 
      T cells to an inflammatory focus. To clarify the role of MCP-1 in the 
      pathogenesis of myocarditis, we have examined the expression of MCP-1 in rat 
      hearts with experimental autoimmune myocarditis (EAM), and have also measured 
      serum levels of MCP-1 in patients with histology-proven acute myocarditis. Lewis 
      rats were immunized with cardiac myosin and were killed 9, 12, 15, 18, 21, 24, 
      27, 30, 33, 36, 42 and 56 days after immunization. Large mononuclear cells in the 
      myocardial interstitium were stained with an anti-MCP-1 antibody. mRNA of MCP-1 
      increased in the hearts of EAM rats from days 15--27 as shown by quantitative 
      reverse transcription-polymerase chain reaction. Serum MCP-1 levels of the rats 
      with EAM were significantly elevated from days 15--24. In the clinical study, 
      serum levels of MCP-1 in 24 patients with acute myocarditis at the time of 
      admission (165.2 +/- 55.8 pg/ml) were significantly (P = 0.0301) elevated 
      compared with those of 20 healthy volunteers (61.8 +/- 10.7 pg/ml). Serum MCP-1 
      levels of 8 fatal cases (371.8 +/- 145.2 pg/ml) were significantly (P = 0.0058) 
      higher than those of 16 cases who survived (65.5 +/- 12.8 pg/ml). In conclusions, 
      MCP-1 may play an important role in the pathogenesis of human acute myocarditis 
      as well as in the progression of rat EAM.
FAU - Fuse, K
AU  - Fuse K
AD  - The First Department of Internal Medicine, Niigata University School of Medicine, 
      Niigata, Japan. koichif@med.niigata-u.ac.jp
FAU - Kodama, M
AU  - Kodama M
FAU - Hanawa, H
AU  - Hanawa H
FAU - Okura, Y
AU  - Okura Y
FAU - Ito, M
AU  - Ito M
FAU - Shiono, T
AU  - Shiono T
FAU - Maruyama, S
AU  - Maruyama S
FAU - Hirono, S
AU  - Hirono S
FAU - Kato, K
AU  - Kato K
FAU - Watanabe, K
AU  - Watanabe K
FAU - Aizawa, Y
AU  - Aizawa Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Chemokine CCL2/biosynthesis/*blood/genetics
MH  - Disease Models, Animal
MH  - Gene Expression
MH  - Humans
MH  - Immunohistochemistry/methods
MH  - Myocarditis/blood/*immunology
MH  - Myocardium/pathology
MH  - RNA, Messenger
MH  - Rats
MH  - Rats, Inbred Lew
PMC - PMC1906075
EDAT- 2001/07/27 10:00
MHDA- 2001/08/31 10:01
PMCR- 2002/06/01
CRDT- 2001/07/27 10:00
PHST- 2001/07/27 10:00 [pubmed]
PHST- 2001/08/31 10:01 [medline]
PHST- 2001/07/27 10:00 [entrez]
PHST- 2002/06/01 00:00 [pmc-release]
AID - cei1510 [pii]
AID - 10.1046/j.1365-2249.2001.01510.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2001 Jun;124(3):346-52. doi: 10.1046/j.1365-2249.2001.01510.x.