scholarly journals Exercise‐Induced Expression of Vascular Endothelial Growth Factor mRNA in Rat Skeletal Muscle is Dependent on Fibre Type

2003 ◽  
Vol 552 (1) ◽  
pp. 213-221 ◽  
Author(s):  
Olivier J. G. Birot ◽  
Nathalie Koulmann ◽  
André Peinnequin ◽  
Xavier A. Bigard
Keyword(s):  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Fibre Type ◽  
Vascular Endothelial ◽  
Rat Skeletal Muscle ◽  
Induced Expression ◽  
Exercise Induced ◽  
Endothelial Growth Factor

scholarly journals Myocyte vascular endothelial growth factor is required for exercise-induced skeletal muscle angiogenesis

2010 ◽  
Vol 299 (4) ◽  
pp. R1059-R1067 ◽  
Author(s):  
I. Mark Olfert ◽  
Richard A. Howlett ◽  
Peter D. Wagner ◽  
Ellen C. Breen
Keyword(s):  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Exercise Training ◽  
Metabolic Adaptation ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Running Speed ◽  
Endothelial Growth Factor ◽  
Adaptation To Exercise

We have previously shown, using a Cre-LoxP strategy, that vascular endothelial growth factor (VEGF) is required for the development and maintenance of skeletal muscle capillarity in sedentary adult mice. To determine whether VEGF expression is required for skeletal muscle capillary adaptation to exercise training, gastrocnemius muscle capillarity was measured in myocyte-specific VEGF gene-deleted (mVEGF−/−) and wild-type (WT) littermate mice following 6 wk of treadmill running (1 h/day, 5 days/wk) at the same running speed. The effect of training on metabolic enzyme activity levels and whole body running performance was also evaluated in mVEGF−/− and WT mice. Posttraining capillary density was significantly increased by 59% ( P < 0.05) in the deep muscle region of the gastrocnemius in WT mice but did not change in mVEGF−/− mice. Maximal running speed and time to exhaustion during submaximal running increased by 20 and 13% ( P < 0.05), respectively, in WT mice after training but were unchanged in mVEGF−/− mice. Training led to increases in skeletal muscle citrate synthase (CS) and phosphofructokinase (PFK) activities in both WT and mVEGF−/− mice ( P < 0.05), whereas β-hydroxyacyl-CoA dehydrogenase (β-HAD) activity was increased only in WT mice. These data demonstrate that skeletal muscle capillary adaptation to physical training does not occur in the absence of myocyte-expressed VEGF. However, skeletal muscle metabolic adaptation to exercise training takes place independent of myocyte VEGF expression.

A new transacting factor that modulates hypoxia-induced expression of the erythropoietin gene

Blood ◽  
2000 ◽  
Vol 96 (2) ◽  
pp. 491-497 ◽  
Author(s):  
Madhu Gupta ◽  
Paul T. Mungai ◽  
Eugene Goldwasser
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Messenger Rna ◽  
Leucine Zipper ◽  
Fetal Liver ◽  
Specific Interaction ◽  
Vascular Endothelial ◽  
Induced Expression ◽  
Murine Homolog ◽  
Endothelial Growth Factor

Abstract Hypoxia is a strong stimulus for the transcription of a set of genes, including erythropoietin and vascular endothelial growth factor. Here we report on the cloning, functional significance, and expression of a complementary DNA (cDNA) that is involved in hypoxia-mediated expression of these 2 genes. The full-length cDNA encodes a predicted protein of 806 amino acids that contains a leucine zipper motif. This protein, termed HAF for hypoxia-associated factor, binds to a 17-base pair (bp) region of the erythropoietin promoter, which was shown earlier to participate in hypoxia-induced expression of the erythropoietin gene. In Hep3B cells, clones modified to express HAF antisense RNA showed an attenuated response to hypoxia-mediated induction of both erythropoietin and vascular endothelial growth factor transcription. HAF showed sequence-specific interaction with a DNA element in the 5′ untranslated region ofVEGF gene. The HAF 2.6-kilobase (kb) messenger RNA (mRNA) is expressed in most adult tissues. The highest expression occurs in fetal liver and the least in adult liver. HAF is the murine homolog of Sart-1, a 125-kd human protein expressed in the nuclei of normal and malignant cells.

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