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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain
THE -AMYLOID INCREASES THE EXPRESSION OF RCAN
Abstract number: P108
Mora1,2 NJ, Lloret1,2 A, Badia1 MC, Dasi3 F, Markovic1,2 J, Pallardo1,2 FV, Vina1 J
1Department of Physiology, Medical School of the University of Valencia, Blasco Ibaez 15, 46010, Valencia, Spain.
2CIBERER, Blasco Ibez, 15, 46010, Valencia, Spain.
3Unidad Central de Investigacion, Medical School of the University of Valencia, Spain. [email protected]
Aim:
The relationship between b-amyloid toxicity and RCAN expression.
Methods:
Glutathione determination by H.P.L.C. and enzymatic essay; Ca+2 level by Fluo-3 marking followed by confocal microscopy, apoptosis detection by annexin V/propidium iodide, the RCAN pathway by PCR, peroxide production by spectrofluorimetry Model: PC12 cell line
Results:
GSH decreased and the level of hydrogen peroxide increased following the incubation with b-amyloid. Ca+2 levels were augmented with respect to the control, as well as the percentage of annexin V positive cells. These results indicate the apoptosis process caused by oxidative stress. The simultaneous administration with GSH ester and Trolox prevents the effect of b-amyloid. PCR results show the induction of the expression of GSK3 b, RCAN 1.4, RCAN 1.1, and calcineurin.
Conclusion:
Our results indicate a new approach in the study of Alzheimer disease. The possible modulation of RCAN pathway mediated by oxidative stress as a consequence of the incubation with b-amyloid, could give a further insight into the mechanism of this pathology.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :P108