PMID- 9024159
OWN - NLM
STAT- MEDLINE
DCOM- 19970311
LR  - 20220227
IS  - 0009-7322 (Print)
IS  - 0009-7322 (Linking)
VI  - 95
IP  - 3
DP  - 1997 Feb 4
TI  - Induction of monocyte chemoattractant protein-1 in the small veins of the 
      ischemic and reperfused canine myocardium.
PG  - 693-700
AB  - BACKGROUND: Healing after myocardial infarction is characterized by the presence 
      of macrophages in the infarcted area. Since augmented monocyte influx has been 
      implicated as a potential mechanism for improved healing after reperfusion, we 
      wished to study the induction of monocyte chemoattractant protein-1 (MCP-1) 
      during reperfusion. METHODS AND RESULTS: The cDNA for MCP-1 was cloned from a 
      canine jugular vein endothelial cell (CJVEC) library and exhibited 78% identity 
      with the deduced amino acid sequence of human MCP-1. Samples of myocardium were 
      taken from control and ischemic segments after 1 hour of ischemia and various 
      times of reperfusion; total RNA was isolated from myocardial samples and probed 
      with a cDNA probe for canine MCP-1. Induction of MCP-1 mRNA occurred only in 
      previously ischemic segments within the first hour of reperfusion, peaked at 3 
      hours, and persisted throughout the first 2 days of reperfusion. In the absence 
      of reperfusion, no significant MCP-1 induction was seen. Both ischemic (but not 
      preischemic) cardiac lymph and human recombinant TNF-alpha induced MCP-1 in 
      CJVECs. MCP-1 was identified by immunostaining on infiltrating cells and venular 
      (but not arterial) endothelium by 3 hours. In contrast, in situ hybridization 
      showed MCP-1 mRNA to be confined to the endothelium of small veins (venules) 10 
      to 70 microns in diameter. CONCLUSIONS: MCP-1 mRNA is induced in the endothelium 
      of a specific class of small veins immediately after reperfusion. MCP-1 induction 
      is confined to the previously ischemic area that has been reperfused. We suggest 
      a significant role for MCP-1 in monocyte trafficking in the reperfused 
      myocardium.
FAU - Kumar, A G
AU  - Kumar AG
AD  - Methodist Hospital, DeBakey Heart Center, Department of Medicine, Houston, TX, 
      USA.
FAU - Ballantyne, C M
AU  - Ballantyne CM
FAU - Michael, L H
AU  - Michael LH
FAU - Kukielka, G L
AU  - Kukielka GL
FAU - Youker, K A
AU  - Youker KA
FAU - Lindsey, M L
AU  - Lindsey ML
FAU - Hawkins, H K
AU  - Hawkins HK
FAU - Birdsall, H H
AU  - Birdsall HH
FAU - MacKay, C R
AU  - MacKay CR
FAU - LaRosa, G J
AU  - LaRosa GJ
FAU - Rossen, R D
AU  - Rossen RD
FAU - Smith, C W
AU  - Smith CW
FAU - Entman, M L
AU  - Entman ML
LA  - eng
GR  - AI-28071/AI/NIAID NIH HHS/United States
GR  - HL-42550/HL/NHLBI NIH HHS/United States
GR  - NS-32583/NS/NINDS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Coronary Vessels/*metabolism
MH  - Dogs
MH  - Endothelium, Vascular/cytology/metabolism
MH  - Female
MH  - Humans
MH  - Jugular Veins/metabolism
MH  - Lymph/metabolism
MH  - Male
MH  - Molecular Sequence Data
MH  - Myocardial Ischemia/*metabolism
MH  - *Myocardial Reperfusion
MH  - RNA, Messenger/metabolism
MH  - Veins
EDAT- 1997/02/04 00:00
MHDA- 1997/02/04 00:01
CRDT- 1997/02/04 00:00
PHST- 1997/02/04 00:00 [pubmed]
PHST- 1997/02/04 00:01 [medline]
PHST- 1997/02/04 00:00 [entrez]
AID - 10.1161/01.cir.95.3.693 [doi]
PST - ppublish
SO  - Circulation. 1997 Feb 4;95(3):693-700. doi: 10.1161/01.cir.95.3.693.