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-independent manner: role of oxygen
radicals
1 Section of Cardiovascular Sciences and Cardiology, Department of Medicine, the DeBakey Heart Center, Baylor College of Medicine, and the Methodist Hospital; 2 Veterans Administration Medical Center, Winters Center for Heart Failure Research, Houston, Texas 77030; and 3 Immunex Corporation, Seattle, Washington 98101
Early chemokine induction in
the area at risk of an ischemic-reperfused (I/R) myocardium is
first seen in the venular endothelium. Reperfusion is associated with
several induction mechanisms including increased extracellular
tumor necrosis factor (TNF)-
, reactive oxygen intermediate (ROI)
species formation, and adhesion of leukocytes to the venular
endothelium. To test the hypothesis that chemokine induction in cardiac
venules can occur by ROIs in a TNF--independent manner, and in the
absence of leukocyte accumulation, we utilized wild-type (WT) and
TNF- double-receptor knockout mice (DKO) in a closed-chest mouse
model of myocardial ischemia (15 min) and reperfusion (3 h), in
which there is no infarction. We demonstrate that a single brief period
of I/R induces significant upregulation of the chemokines macrophage
inflammatory protein (MIP) -1, -1
, and -2 at both the mRNA and
protein levels. This induction was independent of TNF-, whereas
levels of these chemokines were increased in both WT and DKO mice.
Chemokine induction was seen predominantly in the endothelium of
small veins and was accompanied by nuclear translocation of nuclear
factor-
B and c-Jun (AP-1) in venular endothelium. Intravenous
infusion of the oxygen radical scavenger
N-2-mercaptopropionyl glycine (MPG) initiated 15 min before
ischemia and maintained throughout reperfusion obviated chemokine induction, but MPG administration after reperfusion had begun
had no effect. The results suggest that ROI generation in the
reperfused myocardium rapidly induces C-C and C-X-C chemokines in the
venular endothelium in the absence of infarction or irreversible cellular injury.
macrophage inflammatory protein; endothelium; transgenic animals
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