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

  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},
  volume={16 5},
  • M. Infanger, S. Faramarzi, D. Grimm
  • Published 1 September 2007
  • Biology, Medicine
  • Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
Prostaglandin E2 reduces swine myocardial ischemia reperfusion injury via increased endothelial nitric oxide synthase and vascular endothelial growth factor expression levels
The results of the present study demonstrate the cardio-protective mechanisms of PGE2, which may protect the heart from I/R injury via enhancement of VEGF and eNOS expression levels.
Insulin-like growth factor-1 overexpression in cardiomyocytes diminishes ex vivo heart functional recovery after acute ischemia.
  • C. Prêle, M. Reichelt, M. Grounds
  • Medicine, Biology
    Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
  • 2012
Cardioprotective Effect of VEGF and Venom VEGF-like Protein in Acute Myocardial Ischemia in Mice: Effect on Mitochondrial Function
VEGF or ICPP intravenous administration at reperfusion largely reduces IS in IR, through stimulation of VEGFR2 receptors, and this effect is mediated, at least in part, by improvement of IR-induced mitochondrial dysfunction.
A Soluble Receptor for Advanced Glycation End-Products Inhibits Hypoxia/Reoxygenation-Induced Apoptosis in Rat Cardiomyocytes via the Mitochondrial Pathway
It is concluded that the exogenous administration of sRAGE during H/R is involved in cardioprotection by inhibiting apoptosis via the mitochondrial pathway, which, if further confirmed in vivo, may have important clinical implications during H-R.
The Impact of Vascular Endothelial Growth Factor and Basic Fibroblast Growth Factor on Cardiac Fibroblasts Grown under Altered Gravity Conditions
Investigation of the impact of basic fibroblast growth factor and vascular endothelial growth factor on cardiac fibroblasts grown under altered gravity conditions found growth factor treatment attenuated programmed cell death and ECMP secretion.
Effects of ACE inhibition on endothelial progenitor cell mobilization and prognosis after acute myocardial infarction in type 2 diabetic patients
The use of angiotensin-converting enzyme inhibitors represents a novel approach for improving cardiovascular repair after acute myocardial infarction in T2DM patients.
Receptor tyrosine kinase profiling of ischemic heart identifies ROR1 as a potential therapeutic target
In vitro findings suggest a role for ROR1 as a potential target for the treatment of ischemic heart injury, and several novel RTKs were found to be regulated in expression or activity in isChemic heart.
Intramyocardial delivery of VEGF165 via a novel biodegradable hydrogel induces angiogenesis and improves cardiac function after rat myocardial infarction
The results suggest that injection of VEGF165 along with a hydrogel acquires more cardioprotective effects than either alone in rat with MI by sustained release of V EGF165, then may enhance the feedback between VegF and its receptors flk-1 and flt-1.


VEGF, flk-1, and flt-1 expression in a rat myocardial infarction model of angiogenesis.
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.
Upregulation of vascular endothelial growth factor expression induced by myocardial ischaemia: implications for coronary angiogenesis.
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.
Rapid induction of vascular endothelial growth factor expression by transient ischemia in rat heart.
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.
Mechanisms of apoptosis after ischemia and reperfusion: Role of the renin-angiotensin system
The data suggest that the RAS plays a pivotal role in cardiac apoptosis which is the early and predominant form of death in myocardial infarction.
Tissue inhibition of angiotensin-converting enzyme activity stimulates angiogenesis in vivo.
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.
Regional expression of endothelin-1, ANP, IGF-1, and LV wall stress in the infarcted rat heart.
It is concluded that ET-1, ANP, and IGF-1 are expressed in different patterns in the infarcted heart in relation to time, functional regions, cellular distribution, and mechanical load.
Vascular endothelial growth factor up-regulates its receptor fms-like tyrosine kinase 1 (FLT-1) and a soluble variant of FLT-1 in human vascular endothelial cells.
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.