PMID- 10908159
OWN - NLM
STAT- MEDLINE
DCOM- 20000801
LR  - 20230216
IS  - 0023-6837 (Print)
IS  - 0023-6837 (Linking)
VI  - 80
IP  - 7
DP  - 2000 Jul
TI  - Roles and relationship of macrophages and monocyte chemotactic and activating 
      factor/monocyte chemoattractant protein-1 in the ischemic and reperfused rat 
      heart.
PG  - 1127-36
AB  - Reperfusion injury is a troublesome and unresolved problem in acute myocardial 
      infarction and is believed to be associated with inflammatory reactions in which 
      various types of cells and cytokines participate, in particular, macrophages and 
      monocyte chemoattractant protein-1 (MCP-1). We designed this study to clarify the 
      role and relationship of macrophages and MCP-1 in ischemic and reperfused heart. 
      The number and distribution of macrophages and MCP-1 messenger RNA (mRNA) in the 
      ischemic and reperfused rat heart were examined with in situ hybridization and 
      immunohistochemistry. Myocardial samples were obtained at several times. In situ 
      hybridization was performed with digoxigenin-labeled antisense RNA probe for rat 
      MCP-1 mRNA, and immunohistochemistry was performed with antimacrophage antibody. 
      Double staining with in situ hybridization and immunohistochemistry was also 
      performed. The number of MCP-1 mRNA-positive cells increased after reperfusion 
      and peaked at 3 hours after reperfusion. Early infiltration of ischemic tissues 
      by macrophages was also observed at the time of the absence of an increase of 
      MCP-1 mRNA-positive cells, and this infiltration was not significantly 
      accelerated by reperfusion, but by ischemia itself. The numbers of both MCP-1 
      mRNA-positive cells and macrophages increased in the ischemic marginal region 
      over time. From the result of double staining, and based on the cellular 
      morphology and the distribution, the majority of MCP-1 mRNA-positive cells 
      appeared to be activated macrophages. This suggests that macrophages may not be 
      attracted to cardiac tissue only by MCP-1 and that MCP-1 may have some roles 
      other than attracting macrophages into ischemic heart. It also suggests that 
      macrophages and MCP-1 may play an important role in reperfusion injury and that 
      MCP-1 may be one of the key molecules of reperfusion injury. These observations 
      may contribute to the development of a new therapeutic approach to the prevention 
      of reperfusion injury.
FAU - Kakio, T
AU  - Kakio T
AD  - Department of Cardiovascular Medicine, Kyoto University, Japan.
FAU - Matsumori, A
AU  - Matsumori A
FAU - Ono, K
AU  - Ono K
FAU - Ito, H
AU  - Ito H
FAU - Matsushima, K
AU  - Matsushima K
FAU - Sasayama, S
AU  - Sasayama S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Lab Invest
JT  - Laboratory investigation; a journal of technical methods and pathology
JID - 0376617
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/genetics/*physiology
MH  - Immunohistochemistry/methods
MH  - In Situ Hybridization
MH  - Macrophages/*physiology
MH  - Male
MH  - Myocardial Ischemia/metabolism/pathology/*physiopathology
MH  - Myocardial Reperfusion Injury/metabolism/pathology/*physiopathology
MH  - Myocardium/*metabolism/*pathology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Staining and Labeling
EDAT- 2000/07/25 11:00
MHDA- 2000/08/06 11:00
CRDT- 2000/07/25 11:00
PHST- 2000/07/25 11:00 [pubmed]
PHST- 2000/08/06 11:00 [medline]
PHST- 2000/07/25 11:00 [entrez]
AID - S0023-6837(22)02139-0 [pii]
AID - 10.1038/labinvest.3780119 [doi]
PST - ppublish
SO  - Lab Invest. 2000 Jul;80(7):1127-36. doi: 10.1038/labinvest.3780119.