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      Hypoxia is a strong inducer of vascular endothelial growth factor mRNA expression in the heart.

      Biochemical and Biophysical Research Communications
      Animals, Animals, Newborn, Base Sequence, Blotting, Northern, Blotting, Southern, Cell Hypoxia, Cells, Cultured, DNA, analysis, Endothelial Growth Factors, biosynthesis, Fibroblasts, metabolism, Gene Expression, Guinea Pigs, Heart, drug effects, Heart Ventricles, Lymphokines, Molecular Sequence Data, Myocardium, Oligodeoxyribonucleotides, Polymerase Chain Reaction, RNA, Messenger, isolation & purification, Rats, Rats, Wistar, Tetradecanoylphorbol Acetate, pharmacology, Transcription, Genetic, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors

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          Abstract

          Vascular endothelial growth factor (VEGF) is a potent and specific mitogen for vascular endothelial cells. A 3.9 kb VEGF transcript is expressed by all cardiac tissues from rat, mouse and guinea pig examined. VEGF expression was not developmentally regulated. The major form of VEGF mRNAs expressed by cardiac tissues coded for VEGF188. Myocyte enriched and fibroblast enriched cultures of new born rat heart cells also expressed VEGF transcripts but the major mRNA found coded for VEGF164. The expression of VEGF mRNA in myocyte enriched cultures of new born rat ventricles was increased 2 fold by serum, 5 fold by phorbol myristate acetate and 7 fold by hypoxic conditions. We conclude that hypoxic conditions may promote cardiac capillary cell growth by inducing VEGF expression.

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