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Summary
Gasser R et al.  
A Microarray and Real Time PCR Study on the Effect of Experimental Ischemia upon the Expression of the Insulin-Dependent Transmembrane Glucose Transport Molecule GLUT4 in Human Atrial Myocardium

Journal of Clinical and Basic Cardiology 2006; 9 (1-4): 4-9

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Fig. 1: Ischemia Experiments Fig. 2: Glut4 Fig. 3: Real Time PCR



Keywords: GlukoseIschämieMyokardglucoseGLUT4ischaemiamyocardial

Glucose and high energy metabolism play a pivotal role in the development of numerous salient characteristics of myocardial ischemia, such as the gating properties of specific ion-channels, intracellular ion-homeostasis, electrical phenomena, contractility and other phenomena. Many of these aspects of myocardial ischemia are linked in one or the other way to transmembrane glucose transport, intracellular glucose metabolism and, in fact, to GLUT4. In human cardiac tissue (right auricle), we here investigate to which extent GLUT4 gene expression is altered in experimental ischemia. Using microarray technique we first look at general changes in expression profiles during simulated myocardial ischemia, the behaviour of SLC2A4 (GLUT4, solute carrier family 2 [facilitated glucose transporter], member 4) as well as its regulator gene SLC2A4RG. Then, using Real Time PCR (Light Cycler), we quantify GLUT4 mRNA expression changes in 8 single experiments under ischemic and control conditions. Using the microarray technique, we find that both the expression of GLUT4 gene (SLC2A4) and its regulator gene remain practically unchanged. In Real Time PCR (Light Cycler), the mean ratio for GLUT4 gene expression compared to the house keeping gene G6PDH was under well oxygenated conditions –0.0052 ± 0.0203 and under N2-simulated ischemia 0.0179 ± 0.0196 (n = 8; ± SEM). No statistically significant difference could be found between the two groups. Results show a trend to a slight increase in expression, however no statistical significance could be seen. No significant changes are seen in the expression of the GLUT4 gene as well as in its regulatory gene after 30 minutes of N2-mediated experimental ischemia. Similarly, biological processes involved in glucose metabolism are not significantly de-regulated as others are. This, as well as a slight trend towards up-regulation can be interpreted as an attempt of the myocyte to maintain energy metabolism stable under hypoxic conditions.
 
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