PMID- 7954630
OWN - NLM
STAT- MEDLINE
DCOM- 19941221
LR  - 20190512
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 28
IP  - 8
DP  - 1994 Aug
TI  - Expression of intercellular adhesion molecule-1 on rat cardiac myocytes by 
      monocyte chemoattractant protein-1.
PG  - 1258-62
AB  - OBJECTIVE: Cytokine induction of intercellular adhesion molecule-1 (ICAM-1) on 
      cardiac myocytes may be a critical step in cardiac inflammation associated with 
      acute myocardial infarction and myocarditis. The aim of this study was to 
      investigate the involvement of monocyte chemoattractant protein-1 (MCP-1), a 
      homologue of mouse JE, in the neutrophil-myocyte adhesion in vitro. METHODS: 
      MCP-1/JE and ICAM-1 mRNA expression in cultured neonatal rat cardiac myocytes was 
      evaluated by northern blot analysis. ICAM-1 molecule content on myocytes was 
      determined by ELISA. For adherence assay, myocytes and neutrophils were 
      co-incubated and the number of bounded neutrophils was counted. RESULTS: MCP-1/JE 
      transcripts were not clearly observed in cultured neonatal rat cardiac myocytes; 
      however, its transcripts were clearly detected by exposure to interleukin 1 alpha 
      (100 U.ml-1), lipopolysaccharide (1 microgram.ml-1), or hypoxia (95% N2 + 5% 
      CO2). In ELISA analysis, the expression of ICAM-1 molecules on cardiac myocytes 
      was significantly stimulated by MCP-1 in a dose dependent manner, and the effect 
      of MCP-1 was observed as early as at 6 h. In northern blot analysis, ICAM-1 mRNA 
      expression was constitutively observed in myocytes, and the expression was 
      markedly stimulated by exposure to MCP-1 with a peak elevation at 2 h. In 
      adherence assay, MCP-1 stimulated the adhesion of rat neutrophils to rat cardiac 
      myocytes, and this effect of MCP-1 was inhibited by an anti-ICAM-1 MAb. 
      CONCLUSIONS: These results suggest that cardiac myocytes produce MCP-1, which 
      could in turn promote the adhesion of neutrophils to myocytes via ICAM-1 
      expression, suggesting the involvement of MCP-1 in cardiac inflammation 
      associated with acute myocardial infarction and myocarditis.
FAU - Ban, K
AU  - Ban K
AD  - Jichi Medical School, Tochigi, Japan.
FAU - Ikeda, U
AU  - Ikeda U
FAU - Takahashi, M
AU  - Takahashi M
FAU - Kanbe, T
AU  - Kanbe T
FAU - Kasahara, T
AU  - Kasahara T
FAU - Shimada, K
AU  - Shimada K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Cell Adhesion
MH  - Cells, Cultured
MH  - Chemokine CCL2
MH  - Chemotactic Factors/genetics/*pharmacology
MH  - Cytokines/genetics/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Gene Expression
MH  - Intercellular Adhesion Molecule-1/*genetics
MH  - Myocardium/cytology/*metabolism
MH  - Neutrophils/cytology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Stimulation, Chemical
EDAT- 1994/08/01 00:00
MHDA- 1994/08/01 00:01
CRDT- 1994/08/01 00:00
PHST- 1994/08/01 00:00 [pubmed]
PHST- 1994/08/01 00:01 [medline]
PHST- 1994/08/01 00:00 [entrez]
AID - 0008-6363(94)90365-4 [pii]
AID - 10.1093/cvr/28.8.1258 [doi]
PST - ppublish
SO  - Cardiovasc Res. 1994 Aug;28(8):1258-62. doi: 10.1093/cvr/28.8.1258.