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Sang Thrombose Vaisseaux, ISSN 0999-7385, 11/2010, Volume 22, Issue 9, pp. 487 - 492
Journal Article
Sang Thrombose Vaisseaux, ISSN 0999-7385, 11/2009, Volume 21, Issue 9, pp. 494 - 496
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 09/2012, Volume 32, Issue 9, pp. 2206 - 2213
OBJECTIVE—Leukocyte infiltration in ischemic areas is a hallmark of myocardial infarction, and overwhelming infiltration of innate immune cells has been shown... 
immune system | ischemic heart disease | leukocytes | chemokines | inflammation | OXIDATIVE STRESS | DEATH | INDUCTION | SUBSET | ZINC-FINGER PROTEIN | PERIPHERAL VASCULAR DISEASE | MICE | DYSFUNCTION | HEMATOLOGY | EXPRESSION | MCPIP | Receptors, CCR2 - genetics | Inflammation - pathology | Myocardial Infarction - genetics | Myocardium - immunology | Ventricular Function, Left | Humans | Monocytes - immunology | Myocardial Infarction - diagnostic imaging | Neutrophil Infiltration | Myocardial Infarction - immunology | Heart Rupture, Post-Infarction - immunology | Inflammation - metabolism | Matrix Metalloproteinase 9 - metabolism | Ventricular Remodeling | Hypertrophy, Left Ventricular - pathology | Myocardium - metabolism | Bone Marrow Transplantation | Inflammation Mediators - metabolism | Ultrasonography | Antigens, Ly - metabolism | Chemokine CCL3 - metabolism | Myocardial Infarction - physiopathology | Chemokine CCL2 - metabolism | Receptors, Chemokine - genetics | Disease Models, Animal | Receptors, CCR10 - metabolism | Signal Transduction | Matrix Metalloproteinase 2 - metabolism | Mice, Inbred C57BL | Receptors, Chemokine - metabolism | Neutrophils - immunology | Genotype | Myocardium - pathology | Inflammation - immunology | Myocardial Infarction - metabolism | Chemotaxis | Mice, Knockout | Receptors, Chemokine - deficiency | Stroke Volume | Myocardial Infarction - complications | Hypertrophy, Left Ventricular - immunology | Phenotype | Animals | Inflammation - genetics | Inflammation - prevention & control | Mice | Receptors, CCR2 - deficiency | Heart Rupture, Post-Infarction - pathology
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 03/2012, Volume 32, Issue 3, pp. 643 - 653
OBJECTIVE—Catecholamines have been shown to control bone marrow (BM)–derived cell egress, yet the cellular and molecular mechanisms involved in this effect and... 
catecholamines | nitric oxide | nitric oxide synthase | angiogenesis | ischemia | PROGENITOR CELLS | RECRUITMENT | MOBILIZATION | STEM | OVEREXPRESSION | PERIPHERAL VASCULAR DISEASE | NEOVASCULARIZATION | HEMATOLOGY | NEOANGIOGENESIS | EXPRESSION | PROMOTES | Tyrosine 3-Monooxygenase - metabolism | Up-Regulation | Hindlimb | Bone Marrow Cells - enzymology | Sympathetic Nervous System - drug effects | Ischemia - enzymology | Bone Marrow - enzymology | Green Fluorescent Proteins - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Sympathetic Nervous System - metabolism | Adrenergic beta-2 Receptor Agonists - pharmacology | Stromal Cells - enzymology | Ligation | Time Factors | Bone Marrow Transplantation | Bone Marrow Cells - drug effects | Nitric Oxide Synthase Type III - metabolism | Dopamine - metabolism | Bone Marrow - drug effects | Disease Models, Animal | Muscle, Skeletal - blood supply | Dopamine Agonists - pharmacology | Green Fluorescent Proteins - metabolism | Signal Transduction | Endothelial Cells - metabolism | Mice, Inbred C57BL | Cells, Cultured | Enzyme Inhibitors - pharmacology | Mice, Transgenic | Ischemia - physiopathology | Nitric Oxide Synthase Type III - genetics | Mice, Knockout | Nitric Oxide Synthase Type III - antagonists & inhibitors | Cell Movement - drug effects | Tyrosine 3-Monooxygenase - genetics | Animals | Norepinephrine - metabolism | Cell Differentiation - drug effects | Mice | Enzyme Activation | Bone Marrow - innervation | Femoral Artery - surgery | Neovascularization, Physiologic | Endothelial Cells - drug effects
Journal Article
Journal Article
Circulation, ISSN 0009-7322, 07/2009, Volume 120, Issue 1, pp. 50 - 59
Background-The hypoxia-inducible transcription factor (HIF) subunits are destabilized via the O-2-dependent prolyl hydroxylase domain proteins (PHD1, PHD2, and... 
Angiogenesis | Hypoxia | Inflammation | Ischemia | hypoxia | ISCHEMIA-INDUCED ANGIOGENESIS | HIF-1-ALPHA/VP16 HYBRID | CELLS | RECRUITMENT | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | angiogenesis | HYPOXIA-INDUCIBLE-FACTOR | FACTOR-I | ischemia | inflammation | ACUTE MYOCARDIAL-INFARCTION | PERIPHERAL VASCULAR DISEASE | NEOVASCULARIZATION | HEMATOLOGY | HIF-ALPHA | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Mice, Inbred C57BL | Gene Silencing | Ischemia - metabolism | Ischemia - therapy | Hypoxia-Inducible Factor-Proline Dioxygenases | Vascular Endothelial Growth Factor A - metabolism | Ischemia - physiopathology | RNA, Messenger - metabolism | Procollagen-Proline Dioxygenase - metabolism | Neovascularization, Physiologic - physiology | Plasmids - pharmacology | Inflammation - metabolism | Macrophages - metabolism | Animals | Procollagen-Proline Dioxygenase - genetics | Hindlimb - blood supply | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Femoral Artery | Signal Transduction - physiology | Chemokines - metabolism | Mice | Nitric Oxide Synthase Type III - metabolism | Genetic Therapy - methods | Care and treatment | Physiological aspects | Cellular signal transduction | Research | DNA binding proteins | Hydroxylases | Vascular Endothelial Growth Factor A | Hindlimb | Signal Transduction | Gene Therapy | Nitric Oxide Synthase Type III | Macrophages | Hypoxia-Inducible Factor 1, alpha Subunit | Life Sciences | Plasmids | Development Biology | RNA, Messenger | Chemokines | Neovascularization, Physiologic | Procollagen-Proline Dioxygenase
Journal Article
Circulation, ISSN 0009-7322, 2009, Volume 120, Issue 14, pp. 1415 - 1425
Journal Article
Circulation, ISSN 0009-7322, 02/2012, Volume 125, Issue 8, pp. 1014 - 1026
Journal Article
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