Expression of vascular endothelial growth factor and receptor tyrosine kinases in cardiac ischemia/reperfusion injury.

@article{Infanger2007ExpressionOV,
  title={Expression of vascular endothelial growth factor and receptor tyrosine kinases in cardiac ischemia/reperfusion injury.},
  author={Manfred Infanger and Shideh Faramarzi and Jirka Grosse and E J Kurth and Claudia Ulbrich and Johann Bauer and Markus Wehland and Reinhold Kreutz and Peter Walter Kossmehl and Martin Paul and Daniela Grimm},
  journal={Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology},
  year={2007},
  volume={16 5},
  pages={
          291-9
        }
}
  • M. Infanger, S. Faramarzi, D. Grimm
  • Published 1 September 2007
  • Biology, Medicine
  • Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
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TLDR
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TLDR
Acute myocardial infarction is accompanied by rapid and prolonged increase in expression of VEGF and its receptors with characteristic spatial and temporal kinetic, and these findings suggest that the V EGF/VEGF receptor system plays an important role in the angiogenesis and stromal deposition associated with myocardIAL infarctions.
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VEGF production in the myocardium is significantly upregulated by hypoxia in vitro and by ischaemia in vivo, suggesting that VEGF is a likely mediator in the natural process of ischaemic induced myocardial neovascularisation.
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Induction of VEGF mRNA is upregulated by oxygen deprivation in the heart and that not only infarction but also chronic ischemia in the clinical setting could induce VEGf as a potent angiogenesis factor to stimulate coronary collateral formation is suggested.
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TLDR
ACE inhibition with quinaprilat promotes angiogenesis in a rabbit model of hindlimb ischemia and indicates that nonsulfhydryl ACE inhibitors with high tissue affinity may be potentially useful for therapeutic angiogenic in ischemic tissues.
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TLDR
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TLDR
It is shown that media conditioned by various cancer cell lines grown under hypoxic conditions were able to up-regulate expression of FLT-1 mRNA and protein but not of KDR mRNA, which suggests that VEGF itself is the main factor secreted by tumor cells that is able to enhance the expression of its receptor FLt-1 and of a soluble variant of FLS-1 in endothelial cells.
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