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9 resultat
Macrophage overexpression of matrix metalloproteinase-9 in aged mice improves diastolic physiology and cardiac wound healing following myocardial infarction.
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Matrix metalloproteinase (MMP)-9 increases in the myocardium with advanced age and after myocardial infarction (MI). Because young transgenic (TG) mice overexpressing human MMP-9 only in macrophages show better outcomes post-MI, whereas aged TG mice show a worse aging phenotype, we wanted to
Obese and diabetic KKAy mice show increased mortality but improved cardiac function following myocardial infarction.
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BACKGROUND
Introduction of the yellow obese gene (A(y)) into mice (KKAy) results in obesity and diabetes by 5 weeks of age.
METHODS
Using this model of type 2 diabetes, we evaluated male and female 6- to 8-month-old wild-type (WT, n=10) and KKAy (n=22) mice subjected to myocardial infarction (MI)
Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction.
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Matrix metalloproteinases (MMPs) are postulated to be necessary for neovascularization during wound healing. MMP-9 deletion alters remodeling postmyocardial infarction (post-MI), but whether and to what degree MMP-9 affects neovascularization post-MI is unknown. Neovascularization was evaluated in
Morphological characteristics of the microvasculature in healing myocardial infarcts.
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Myocardial infarction (MI) is associated with an angiogenic response, critical for healing and cardiac repair. Using a canine model of myocardial ischemia and reperfusion, we examined the structural characteristics of the evolving microvasculature in healing MI. After 7 days of reperfusion, the
Adipose stromal vascular fraction cell construct sustains coronary microvascular function after acute myocardial infarction.
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A three-dimensional tissue construct was created using adipose-derived stromal vascular fraction (SVF) cells and evaluated as a microvascular protection treatment in a myocardial infarction (MI) model. This study evaluated coronary blood flow (BF) and global left ventricular function after MI with
Temporal profile of microglial response following transient (2 h) middle cerebral artery occlusion.
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We measured the time-dependent morphological changes of microglial cells reacting to ischemic cell damage after transient (2 h) middle cerebral artery occlusion in the rat by means of lectin histochemistry with the B4-isolectin from Griffonia simplicifolia as well as immunohistochemistry with
Impairment of myocardial angiogenic response in the absence of osteopontin.
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OBJECTIVE
Osteopontin (OPN), increased in the heart following myocardial infarction (MI), plays an important role in post-MI remodeling. Angiogenesis, an important feature of tissue repair, begins in the infarcted myocardium within 3 days post-MI. Here, the authors studied the role of OPN in
Characterization of microglial reaction after middle cerebral artery occlusion in rat brain.
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We have studied the microglial reaction that accompanies cortical infarction induced by middle cerebral artery occlusion (MCAO). Lectin histochemistry with the B4-isolectin from Griffonia simplicifolia as well as immunocytochemistry with a panel of monoclonal antibodies directed against major
Online monitoring of myocardial bioprosthesis for cardiac repair.
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OBJECTIVE
The aim of this study was to develop a myocardial bioprosthesis for cardiac repair with an integrated online monitoring system. Myocardial infarction (MI) causes irreversible myocyte loss and scar formation. Tissue engineering to reduce myocardial scar size has been tested with variable
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