TNF-α mediated increase of HIF-1α inhibits VASP expression, which reduces alveolar-capillary barrier function during Acute Lung Injury (ALI)

PLoS ONE

Volumn 9, Issue 7, 2014, Pages

  Tang, Mengjie ^a,b   Tian, Yihao ^a   Li, Doulin ^a   Lv, Jiawei ^c   Li, Qun ^d   Kuang, Changchun ^a   Hu, Pengchao ^a   Wang, Ying ^a   Wang, Jing ^a   Su, Ke ^d   Wei, Lei ^a  

^a WUHAN UNIVERSITY   (China)

^b HUNAN CANCER HOSPITAL   (China)

^c ZHONGNAN HOSPITAL OF WUHAN UNIVERSITY   (China)

^d RENMIN HOSPITAL OF WUHAN UNIVERSITY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

COBALT CHLORIDE; EVANS BLUE; HYPOXIA INDUCIBLE FACTOR 1ALPHA; LIPOPOLYSACCHARIDE; TUMOR NECROSIS FACTOR ALPHA; VASODILATOR STIMULATED PHOSPHOPROTEIN; ACTIN BINDING PROTEIN; CELL ADHESION MOLECULE; PHOSPHOPROTEIN; VASODILATOR-STIMULATED PHOSPHOPROTEIN;

ACUTE LUNG INJURY; ALVEOLAR CAPILLARY BARRIER; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL MEMBRANE PERMEABILITY; CELL VIABILITY; CONCENTRATION (PARAMETERS); CONTROLLED STUDY; DOWN REGULATION; HUMAN; HUMAN CELL; LUNG GAS EXCHANGE; LUNG PARENCHYMA; MOUSE; NONHUMAN; NUCLEOTIDE SEQUENCE; PROTEIN EXPRESSION; PROTEIN FUNCTION; SERUM; SIGNAL TRANSDUCTION; TIGHT JUNCTION; ANIMAL; BAGG ALBINO MOUSE; CAPILLARY; CELL SURVIVAL; CHEMICALLY INDUCED; DOSE RESPONSE; DRUG EFFECTS; GENE EXPRESSION; GENETICS; LUNG ALVEOLUS; METABOLISM; PATHOPHYSIOLOGY; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; RNA INTERFERENCE; SECRETION (PROCESS); TUMOR CELL LINE; VASCULARIZATION; WESTERN BLOTTING;

ACUTE LUNG INJURY; ANIMALS; BLOTTING, WESTERN; CAPILLARIES; CELL ADHESION MOLECULES; CELL LINE, TUMOR; CELL MEMBRANE PERMEABILITY; CELL SURVIVAL; DOSE-RESPONSE RELATIONSHIP, DRUG; GENE EXPRESSION; HUMANS; HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT; LIPOPOLYSACCHARIDES; MICE, INBRED BALB C; MICROFILAMENT PROTEINS; PHOSPHOPROTEINS; PULMONARY ALVEOLI; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RNA INTERFERENCE; TUMOR NECROSIS FACTOR-ALPHA;

EID: 84904608609     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0102967     Document Type: Article

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