Absence of cyclooxygenase-2 exacerbates hypoxia-induced pulmonary hypertension and enhances contractility of vascular smooth muscle cells

Circulation

Volumn 117, Issue 16, 2008, Pages 2114-2122

  Fredenburgh, Laura E ^a   Liang, Olin D ^b   Macias, Alvaro A ^a   Polte, Thomas R ^b   Liu, Xiaoli ^a   Riascos, Dario F ^a   Chung, Su Wol ^a   Schissel, Scott L ^a   Ingber, Donald E ^b   Mitsialis, S Alex ^b   Kourembanas, Stella ^b   Perrella, Mark A ^a  

^a BRIGHAM AND WOMEN S HOSPITAL   (United States)

^b BOSTON CHILDREN S HOSPITAL   (United States)

Author keywords

Hypertension, pulmonary; Hypertrophy; Hypoxia; Prostaglandins; Remodeling; Vasculature

Indexed keywords

CYCLOOXYGENASE 2; ENDOTHELIN 1; ILOPROST; COLLAGEN; ENDOTHELIN A RECEPTOR; PROSTAGLANDIN E2; PTGS2 PROTEIN, MOUSE; VASODILATOR AGENT;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTERIOLE; ARTICLE; CELL PROLIFERATION; CONTROLLED STUDY; DISEASE EXACERBATION; EMBRYO; ENZYME INHIBITION; EXTRACELLULAR MATRIX; FORCE; HEART RIGHT VENTRICLE HYPERTROPHY; HYPOXIA; IN VITRO STUDY; LUNG; LUNG BLOOD VESSEL; MOUSE; MUSCLE CONTRACTILITY; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PULMONARY ARTERY; PULMONARY HYPERTENSION; SMOOTH MUSCLE FIBER; SYSTOLIC BLOOD PRESSURE; UPREGULATION; VASCULAR SMOOTH MUSCLE; WILD TYPE; ANIMAL; ANOXIA; BLOOD PRESSURE; CELL CULTURE; CHRONIC DISEASE; CYTOLOGY; DRUG EFFECT; ENZYMOLOGY; GEL; GENETICS; METABOLISM; MOUSE MUTANT; MUSCLE CONTRACTION; PATHOPHYSIOLOGY; PHYSIOLOGY; TRACTION THERAPY; VASOCONSTRICTION;

ANIMALS; ANOXIA; BLOOD PRESSURE; CELLS, CULTURED; CHRONIC DISEASE; COLLAGEN; CYCLOOXYGENASE 2; DINOPROSTONE; ENDOTHELIN-1; GELS; HYPERTENSION, PULMONARY; HYPERTROPHY, RIGHT VENTRICULAR; ILOPROST; MICE; MICE, MUTANT STRAINS; MUSCLE CONTRACTION; MUSCLE, SMOOTH, VASCULAR; PULMONARY ARTERY; RECEPTOR, ENDOTHELIN A; TRACTION; VASOCONSTRICTION; VASODILATOR AGENTS;

EID: 42449111363     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/CIRCULATIONAHA.107.716241     Document Type: Article

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