Inhibition of vascular calcification by block of intermediate conductance calcium-activated potassium channels with TRAM-34

Pharmacological Research

Volumn 85, Issue , 2014, Pages 6-14

  Freise, Christian ^a   Querfeld, Uwe ^a  

^a CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

Author keywords

KCa3.1; NF B; TNF ; TRAM 34; Vascular calcification; VSMC

Indexed keywords

1 [(2 CHLOROPHENYL)DIPHENYLMETHYL] 1H PYRAZOLE; ALKALINE PHOSPHATASE; CALCIUM; GELATINASE A; GELATINASE B; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; MARKER; MESSENGER RNA; NITRIC OXIDE; OSTEOCALCIN; POTASSIUM CHANNEL; POTASSIUM CHANNEL KCA3.1; SMALL INTERFERING RNA; TRANSCRIPTION FACTOR OSTERIX; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; INTERMEDIATE CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNEL; OSTEOPONTIN; OSTERIX PROTEIN, RAT; PHOSPHATE; POTASSIUM CHANNEL BLOCKING AGENT; PYRAZOLE DERIVATIVE; TRANSCRIPTION FACTOR; TRANSFORMING GROWTH FACTOR BETA;

ANIMAL CELL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BLOOD VESSEL CALCIFICATION; CALCIUM CELL LEVEL; CONTROLLED STUDY; ENZYME ASSAY; ENZYME RELEASE; GENE SILENCING; LUCIFERASE ASSAY; MOUSE; NONHUMAN; PHENOTYPIC VARIATION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; RAT; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; SMOOTH MUSCLE FIBER; VASCULAR SMOOTH MUSCLE CELL; ANIMAL; ANTAGONISTS AND INHIBITORS; CELL CULTURE; CELL LINE; CHEMICALLY INDUCED; CYTOLOGY; DRUG EFFECTS; GENE EXPRESSION; GENETICS; METABOLISM; THORACIC AORTA; VASCULAR CALCIFICATION;

ALKALINE PHOSPHATASE; ANIMALS; AORTA, THORACIC; APOPTOSIS; CALCIUM; CELL LINE; CELLS, CULTURED; GENE EXPRESSION; GENE SILENCING; INTERMEDIATE-CONDUCTANCE CALCIUM-ACTIVATED POTASSIUM CHANNELS; MATRIX METALLOPROTEINASE 2; MATRIX METALLOPROTEINASE 9; MICE; MYOCYTES, SMOOTH MUSCLE; NITRIC OXIDE; OSTEOCALCIN; OSTEOPONTIN; PHOSPHATES; POTASSIUM CHANNEL BLOCKERS; PYRAZOLES; RATS; TRANSCRIPTION FACTORS; TRANSFORMING GROWTH FACTOR BETA; TUMOR NECROSIS FACTOR-ALPHA; VASCULAR CALCIFICATION;

EID: 84902546895     PISSN: 10436618     EISSN: 10961186     Source Type: Journal    
DOI: 10.1016/j.phrs.2014.04.013     Document Type: Article

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