STAT4 deficiency protects against neointima formation following arterial injury in mice

Journal of Molecular and Cellular Cardiology

Volumn 74, Issue , 2014, Pages 284-294

  Lv, Lei ^a   Meng, Qiurong ^a   Ye, Meng ^a   Wang, Peng ^a   Xue, Guanhua ^a  

^a SHANGHAI JIAO TONG UNIVERSITY SCHOOL OF MEDICINE   (China)

Author keywords

Apoptosis; Migration; Restenosis; Signal transducer and activator of transcription 4; Vascular smooth muscle cell

Indexed keywords

CASPASE 3; CYTOCHROME C; FAS ANTIGEN; FAS ASSOCIATED DEATH DOMAIN PROTEIN; GELATINASE; GELATINASE A; INTERSTITIAL COLLAGENASE; MONOCYTE CHEMOTACTIC PROTEIN 1; STAT4 PROTEIN; TUMOR NECROSIS FACTOR RECEPTOR 1; CASP3 PROTEIN, MOUSE; CCL2 PROTEIN, MOUSE; COLLAGENASE 3; MMP13 PROTEIN, MOUSE; MMP2 PROTEIN, MOUSE; STAT4 PROTEIN, MOUSE;

ANIMAL CELL; ANIMAL EXPERIMENT; APOPTOSIS; ARTERY INJURY; ARTICLE; ATHEROSCLEROSIS; CELL CULTURE; CELL HYPERPLASIA; CELL ISOLATION; CELL MIGRATION; CELL PROLIFERATION; CONFOCAL MICROSCOPY; CONTROLLED STUDY; CYTOSOL; ENZYME ACTIVATION; ENZYME RELEASE; FEMORAL ARTERY; IMMUNOHISTOCHEMISTRY; INFLAMMATORY CELL; MOUSE; NEOINTIMA; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEFICIENCY; PROTEIN FUNCTION; PROTEIN PHOSPHORYLATION; RESTENOSIS; SMOOTH MUSCLE FIBER; VASCULAR SMOOTH MUSCLE; WESTERN BLOTTING; WOUND HEALING; ADENOVIRIDAE; ANIMAL; BAGG ALBINO MOUSE; BLOOD VESSEL INJURY; CELL MOTION; DEFICIENCY; GENE EXPRESSION REGULATION; GENE VECTOR; GENETICS; INJURIES; INTIMA; KNOCKOUT MOUSE; METABOLISM; MITOCHONDRION; PATHOLOGY; PRIMARY CELL CULTURE; SIGNAL TRANSDUCTION; THORACIC AORTA;

ADENOVIRIDAE; ANIMALS; AORTA, THORACIC; APOPTOSIS; CASPASE 3; CELL MOVEMENT; CHEMOKINE CCL2; GENE EXPRESSION REGULATION; GENETIC VECTORS; MATRIX METALLOPROTEINASE 13; MATRIX METALLOPROTEINASE 2; MICE; MICE, INBRED BALB C; MICE, KNOCKOUT; MITOCHONDRIA; MUSCLE, SMOOTH, VASCULAR; MYOCYTES, SMOOTH MUSCLE; NEOINTIMA; PRIMARY CELL CULTURE; SIGNAL TRANSDUCTION; STAT4 TRANSCRIPTION FACTOR; TUNICA INTIMA; VASCULAR SYSTEM INJURIES; WOUND HEALING;

EID: 84904727190     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2014.06.001     Document Type: Article

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