TGF-β1-induced thrombospondin-1 expression through the p38 MAPK pathway is abolished by fluvastatin in human coronary artery smooth muscle cells

Vascular Pharmacology

Volumn 44, Issue 6, 2006, Pages 469-475

  McGillicuddy, Fiona C ^a   O'Toole, Daniel ^a   Hickey, Jennifer A ^a   Gallagher, William M ^a   Dawson, Kenneth A ^a   Keenan, Alan K ^a  

^a UNIVERSITY COLLEGE DUBLIN   (Ireland)

Author keywords

Fluvastatin; Human coronary artery smooth muscle cells; Intimal hyperplasia; Thrombospondin 1; Transforming growth factor 1

Indexed keywords

4 (4 FLUOROPHENYL) 2 (4 METHYLSULFINYLPHENYL) 5 (4 PYRIDYL)IMIDAZOLE; ANTHRA[1,9 CD]PYRAZOL 6(2H) ONE; FLUINDOSTATIN; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; MESSENGER RNA; MITOGEN ACTIVATED PROTEIN KINASE P38; THROMBOSPONDIN 1; TRANSFORMING GROWTH FACTOR BETA1; ENZYME INHIBITOR; IMIDAZOLE DERIVATIVE; INDOLE DERIVATIVE; MONOUNSATURATED FATTY ACID; PYRIDINE DERIVATIVE; TGFB1 PROTEIN, HUMAN; TRANSFORMING GROWTH FACTOR BETA;

ADULT; ARTERY INTIMA PROLIFERATION; ARTICLE; CONTROLLED STUDY; CORONARY ARTERY; DRUG EFFECT; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; HUMAN; HUMAN CELL; MALE; PRIORITY JOURNAL; PROTEIN EXPRESSION; RESTENOSIS; SIGNAL TRANSDUCTION; SMOOTH MUSCLE FIBER; VASCULAR SMOOTH MUSCLE; CELL CULTURE; CORONARY BLOOD VESSEL; DOSE RESPONSE; ENZYMOLOGY; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; PHOSPHORYLATION;

ADULT; CELLS, CULTURED; CORONARY RESTENOSIS; CORONARY VESSELS; DOSE-RESPONSE RELATIONSHIP, DRUG; ENZYME INHIBITORS; FATTY ACIDS, MONOUNSATURATED; GENE EXPRESSION REGULATION; HUMANS; HYDROXYMETHYLGLUTARYL-COA REDUCTASE INHIBITORS; IMIDAZOLES; INDOLES; MALE; MAP KINASE SIGNALING SYSTEM; MUSCLE, SMOOTH, VASCULAR; MYOCYTES, SMOOTH MUSCLE; P38 MITOGEN-ACTIVATED PROTEIN KINASES; PHOSPHORYLATION; PYRIDINES; RNA, MESSENGER; THROMBOSPONDIN 1; TRANSFORMING GROWTH FACTOR BETA; TRANSFORMING GROWTH FACTOR BETA1;

EID: 33646773896     PISSN: 15371891     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.vph.2006.03.002     Document Type: Article

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