Activated platelets from diabetic rats cause endothelial dysfunction by decreasing Akt/endothelial NO synthase signaling pathway

PLoS ONE

Volumn 9, Issue 7, 2014, Pages

  Ishida, Keiko ^a   Taguchi, Kumiko ^a   Matsumoto, Takayuki ^a   Kobayashi, Tsuneo ^a  

^a HOSHI UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

ACETYLCHOLINE; BETA3 INTEGRIN; ENDOTHELIAL NITRIC OXIDE SYNTHASE; NITRIC OXIDE; NITROPRUSSIDE SODIUM; PADGEM PROTEIN; PROTEIN KINASE B; THROMBOXANE B2; NITRIC OXIDE SYNTHASE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTERY DILATATION; ARTICLE; CAROTID ARTERY; CONTROLLED STUDY; DIMERIZATION; ENDOTHELIAL DYSFUNCTION; ENZYME INACTIVATION; HUMAN; HUMAN CELL; MALE; NONHUMAN; OXIDATIVE STRESS; PROTEIN EXPRESSION; RAT; SIGNAL TRANSDUCTION; STREPTOZOTOCIN-INDUCED DIABETES MELLITUS; THROMBOCYTE ACTIVATION; ANIMAL; BLOOD; COMPLICATION; EXPERIMENTAL DIABETES MELLITUS; METABOLISM; PATHOLOGY; THROMBOCYTE; VASCULAR DISEASES; VASCULAR ENDOTHELIUM; WISTAR RAT;

ANIMALS; BLOOD PLATELETS; CAROTID ARTERIES; DIABETES MELLITUS, EXPERIMENTAL; ENDOTHELIUM, VASCULAR; MALE; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; OXIDATIVE STRESS; PLATELET ACTIVATION; PROTO-ONCOGENE PROTEINS C-AKT; RATS; RATS, WISTAR; SIGNAL TRANSDUCTION; VASCULAR DISEASES;

EID: 84904568806     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0102310     Document Type: Article

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