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Acta Physiologica 2012; Volume 205, Supplement 690
Joint Meeting of the Hungarian Biophysical Society, Hungarian Physiological Society, Hungarian Society of Anatomists and Hungarian Society of Microcirculation & Vascular Biology
6/11/2012-6/13/2012
Debrecen, Hungary
PROTEOMIC ANALYSIS OF ACUTE RENAL FAILURE CAUSED BY ISHAEMIA/REPERFUSION: IDENTIFICATION OF NEW TARGETS
Abstract number: P45
Sziksz1 E, Himer1 L, Kekesi2 K, Juhasz2 G, Simor2 A, Gulyassy2 P, Darula3 Zs, Szebeni1 B, Tulassay1 T, Vannay1 Á
1MTA-SE Gyermekgygyszati s Nephrolgiai Kutatcsoport s I.sz Gyermekgygyszati Klinika, SE, Budapest, Hungary
2Research Group of Proteomics, Etvs Lrnd University, Budapest, Hungary
3Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary
Background:
Ischaemia/reperfusion (I/R) injury is a leading cause of acute kidney failure (ARF), which is observed most frequently in patients after major surgery, burns, severe hypovolemia, and renal transplantation. Mortality rate and treatment of ARF means a serious problem in the intensive health care. During ischaemia the decreasing oxigen level leads to cell death of renal tubule ad endothelial cells and inflammation. Ischaemic preconditioning (IP) may induce tissue adaptation to stress and protect it from a subsequent severe I/R insult.
Aim:
Because the complex molecular pathomechanism of renal I/R injury is not fully understood, our present aim was to analyse I/R and IP induced protein changes in the kidney to find potential key molecules and therapeutic targets.
Methods:
Proteins from the kidneys of ischemized, preconditioned, preconditioned/ischemized and control rats were isolated and analyzed using two dimensional gel electrophoresis and mass spectrometry. Functional protein analysis was performed by Pathway Studio software. Our selected target molecules will be further analyzed by real-time RT-PCR, western blot and immunofluorescent staining in the future. Furthermore we also plan in vitro experiments.
Results:
108 proteins were altered after insult. They were ranked into functional groups: components of cytoskeleton, elements of different metabolism, proteolysis, DNA/RNA processing, signaling and miscellaneous. All proteins were manually validated and searched in the literature. Some proteins of interest were choosen for further experiments, such as DJ1/PARK7, which may exert cytoprotective effects.
Conclusion:
Here we investigate the alteration in the complex interaction of different proteins of the kidney during ARF. Our results may contribute to the better understanding of the pathomechanism of I/R injury leading to kidney damage. Determination of the protective IP induced proteomic changes will help us to identify new biomarkers and find potential new targets for therapeutic intervention.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 205, Supplement 690 :P45