title: Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium.
abstract: 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.
  
  
  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.
authors.affiliation: Methodist Hospital, DeBakey Heart Center, Department of Medicine, Houston, TX, USA.
authors.forename: A G
authors.initials: AG
authors.lastname: Kumar
authors.forename: C M
authors.initials: CM
authors.lastname: Ballantyne
authors.forename: L H
authors.initials: LH
authors.lastname: Michael
authors.forename: G L
authors.initials: GL
authors.lastname: Kukielka
authors.forename: K A
authors.initials: KA
authors.lastname: Youker
authors.forename: M L
authors.initials: ML
authors.lastname: Lindsey
authors.forename: H K
authors.initials: HK
authors.lastname: Hawkins
authors.forename: H H
authors.initials: HH
authors.lastname: Birdsall
authors.forename: C R
authors.initials: CR
authors.lastname: MacKay
authors.forename: G J
authors.initials: GJ
authors.lastname: LaRosa
authors.forename: R D
authors.initials: RD
authors.lastname: Rossen
authors.forename: C W
authors.initials: CW
authors.lastname: Smith
authors.forename: M L
authors.initials: ML
authors.lastname: Entman
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D003331:Coronary Vessels / Q000378:metabolism*; D004285:Dogs; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D005260:Female; D006801:Humans; D007601:Jugular Veins / Q000378:metabolism; D008196:Lymph / Q000378:metabolism; D008297:Male; D008969:Molecular Sequence Data; D017202:Myocardial Ischemia / Q000378:metabolism*; D015425:Myocardial Reperfusion; D012333:RNA, Messenger / Q000378:metabolism; D014680:Veins
chemical_list: D018932:Chemokine CCL2; D012333:RNA, Messenger