Human plasminogen kringle1-5 reduces atherosclerosis and neointima formation in mice by suppressing the inflammatory signaling pathway

Journal of Thrombosis and Haemostasis

Volumn 8, Issue 1, 2010, Pages 194-201

  Chang, P C ^a,b   Wu, H L ^c   Lin, H C H ^a   Wang, K C ^b   Shi, G Y ^c  

^a Department of Biochemistry and Molecular Biology ^*  (Taiwan)

^b Institute of Molecular and Cellular Biology   (Taiwan)

^c NATIONAL CHENG KUNG UNIVERSITY   (Taiwan)

Author keywords

Atherosclerosis; Kringle 1 5; Neointima formation; Reactive oxygen species

Indexed keywords

ANGIOSTATIN; APOLIPOPROTEIN E; HUMAN PLASMINOGEN KRINGLE 1 5; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INTERCELLULAR ADHESION MOLECULE 1; PLASMINOGEN; REACTIVE OXYGEN METABOLITE; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; VASCULAR CELL ADHESION MOLECULE 1; AUTACOID; I KAPPA B; NF KAPPAB INHIBITOR ALPHA; NF-KAPPAB INHIBITOR ALPHA; PEPTIDE FRAGMENT; PLASMINOGEN KRINGLE 5; RECOMBINANT PROTEIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; AORTA ATHEROSCLEROSIS; ARTERY INTIMA PROLIFERATION; ARTICLE; CAROTID ARTERY LIGATION; COMMON CAROTID ARTERY; CONTROLLED STUDY; DISEASE SEVERITY; DOWN REGULATION; DRUG MECHANISM; ENDOTHELIUM CELL; HUMAN; HUMAN CELL; INFLAMMATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; UMBILICAL VEIN; ANIMAL; AORTA; ATHEROSCLEROSIS; C57BL MOUSE; CAROTID ARTERY; CELL CULTURE; DISEASE MODEL; GENETICS; HYPERPLASIA; IMMUNOLOGY; INTIMA; METABOLISM; MOUSE MUTANT; PATHOLOGY;

ANIMALS; AORTA; APOLIPOPROTEINS E; ATHEROSCLEROSIS; CAROTID ARTERIES; CELLS, CULTURED; DISEASE MODELS, ANIMAL; ENDOTHELIAL CELLS; HUMANS; HYPERPLASIA; I-KAPPA B PROTEINS; INFLAMMATION; INFLAMMATION MEDIATORS; INTERCELLULAR ADHESION MOLECULE-1; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NF-KAPPA B; PEPTIDE FRAGMENTS; PLASMINOGEN; REACTIVE OXYGEN SPECIES; RECOMBINANT PROTEINS; SIGNAL TRANSDUCTION; TUMOR NECROSIS FACTOR-ALPHA; TUNICA INTIMA; VASCULAR CELL ADHESION MOLECULE-1;

EID: 73049107015     PISSN: 15387933     EISSN: 15387836     Source Type: Journal    
DOI: 10.1111/j.1538-7836.2009.03671.x     Document Type: Article

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