Absence of akt1 reduces vascular smooth muscle cell migration and survival and induces features of plaque vulnerability and cardiac dysfunction during atherosclerosis

Arteriosclerosis, Thrombosis, and Vascular Biology

Volumn 29, Issue 12, 2009, Pages 2033-2040

  Fernández Hernando, Carlos ^a,b   József, Levente ^a   Jenkins, Deborah ^a   Di Lorenzo, Annarita ^a   Sessa, William C ^a  

^a YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b NEW YORK UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Akt1; Apoptosis susceptibility; Atherosclerosis; Cardiac dysfunction; Cell migration

Indexed keywords

AKT 1 PROTEIN; COLLAGEN; GELATINASE A; LIPOCORTIN 5; PROTEIN KINASE B; RAC1 PROTEIN; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; ATHEROSCLEROSIS; ATHEROSCLEROTIC PLAQUE; CELL MIGRATION; CELL PROLIFERATION; CELL SURVIVAL; CORONARY ARTERY DISEASE; ECHOCARDIOGRAPHY; ENZYME ACTIVITY; FLOW CYTOMETRY; HEART FUNCTION; HEART INFARCTION; IMMUNOHISTOCHEMISTRY; MALE; MOUSE; NONHUMAN; OXIDATIVE STRESS; PHENOTYPE; PRIORITY JOURNAL; PROTEIN SECRETION; STAINING; STARVATION; VASCULAR SMOOTH MUSCLE;

ANIMALS; APOLIPOPROTEINS E; APOPTOSIS; ATHEROSCLEROSIS; CELL MOVEMENT; CELL PROLIFERATION; CELL SURVIVAL; CELLS, CULTURED; DISEASE MODELS, ANIMAL; HEART; MALE; MAP KINASE SIGNALING SYSTEM; MATRIX METALLOPROTEINASE 2; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MUSCLE, SMOOTH, VASCULAR; MYOCARDIAL INFARCTION; MYOCYTES, SMOOTH MUSCLE; OXIDATIVE STRESS; P21-ACTIVATED KINASES; PLATELET-DERIVED GROWTH FACTOR; PROTO-ONCOGENE PROTEINS C-AKT; RAC GTP-BINDING PROTEINS;

EID: 73849128842     PISSN: 10795642     EISSN: None     Source Type: Journal    
DOI: 10.1161/ATVBAHA.109.196394     Document Type: Article

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