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Text
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URL Address
<a href="http://doi.org/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.01330.2006</a>
Pages
H2729–2736
Issue
6
Volume
292
Dublin Core
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Title
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Optimal reactive oxygen species concentration and p38 MAP kinase are required for coronary collateral growth.
Publisher
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American journal of physiology. Heart and circulatory physiology
Date
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2007
2007-06
Subject
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*Collateral Circulation/drug effects; *Coronary Circulation/drug effects; *MAP Kinase Signaling System/drug effects; Acetophenones/pharmacology; Animal; Animals; Blood Flow Velocity; Cells; Coronary Vessels/surgery; Cultured; Disease Models; Ditiocarb/pharmacology; Endothelial Cells/drug effects/enzymology/*metabolism; Enzyme Inhibitors/pharmacology; Humans; Imidazoles/pharmacology; Inbred WKY; Ligation; Male; Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology; NADPH Oxidases/antagonists & inhibitors/metabolism; Neovascularization; Onium Compounds/pharmacology; Oxygenases/antagonists & inhibitors/metabolism; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism; Physiologic; Pyridines/pharmacology; Rats; Reactive Oxygen Species/*metabolism; Superoxide Dismutase/antagonists & inhibitors/metabolism; Vascular Endothelial Growth Factor A/metabolism
Creator
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Rocic Petra; Kolz Christopher; Reed Ryan; Potter Barry; Chilian William M
Description
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Reactive oxygen species (ROS) are implicated in coronary collateral growth (CCG). We evaluated the requirement for ROS in human coronary artery endothelial cell (HCAEC) tube formation, CCG in vivo, and signaling (p38 MAP kinase) by which ROS may stimulate vascular growth. The flavin-containing oxidase inhibitor diphenyleneiodonium (DPI) or the superoxide dismutase inhibitor diethyldithiocarbamate (DETC) blocked vascular endothelial growth factor-induced HCAEC tube formation in Matrigel. We assessed the effect of DPI and DETC on CCG in a rat model of repetitive ischemia (RI) (40 s left anterior descending coronary artery occlusion every 20 min for 2 h 20 min, 3 times/day, 10 days). DPI or DETC was given intraperitoneally, or the NAD(P)H oxidase inhibitor apocynin was given in drinking water. Collateral-dependent flow (measured by using microspheres) was expressed as a ratio of normal and ischemic zone flows. In sham-operated rats, collateral flow in the ischemic zone was 18 +/- 6% of normal zone; in the RI group, collateral flow in the ischemic zone was 83 +/- 5% of normal zone. DPI prevented the increase in collateral flow after RI (25 +/- 4% of normal zone). Similar results were obtained with apocynin following RI (32 +/- 7% of that in the normal zone). DETC achieved similar results (collateral flow after RI was 21 +/- 2% of normal zone). DPI and DETC blocked RI-induced p38 MAP kinase activation in response to vascular endothelial growth factor and RI. These results demonstrate a requirement for optimal ROS concentration in HCAEC tube formation, CCG, and p38 MAP kinase activation. p38 MAP kinase inhibition prevented HCAEC tube formation and partially blocked RI-induced CCG (42 +/- 7% of normal zone flow), indicating that p38 MAP kinase is a critical signaling mediator of CCG.
Identifier
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<a href="http://doi.org/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.01330.2006</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Collateral Circulation/drug effects
*Coronary Circulation/drug effects
*MAP Kinase Signaling System/drug effects
2007
Acetophenones/pharmacology
American journal of physiology. Heart and circulatory physiology
Animal
Animals
Blood Flow Velocity
Cells
Chilian William M
Coronary Vessels/surgery
Cultured
Department of Integrative Medical Sciences
Disease Models
Ditiocarb/pharmacology
Endothelial Cells/drug effects/enzymology/*metabolism
Enzyme Inhibitors/pharmacology
Humans
Imidazoles/pharmacology
Inbred WKY
Kolz Christopher
Ligation
Male
Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology
NADPH Oxidases/antagonists & inhibitors/metabolism
NEOMED College of Medicine
Neovascularization
Onium Compounds/pharmacology
Oxygenases/antagonists & inhibitors/metabolism
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism
Physiologic
Potter Barry
Pyridines/pharmacology
Rats
Reactive Oxygen Species/*metabolism
Reed Ryan
Rocic Petra
Superoxide Dismutase/antagonists & inhibitors/metabolism
Vascular Endothelial Growth Factor A/metabolism