Structural modifications of NAP-22 in the brain of spontaneously hypertensive rats
https://doi.org/10.18705/1607-419X-2011-17-4-342-346
Abstract
Background. The spontaneously hypertensive rat (SHR) strain is the most common animal model both of hypertension and of cognitive impairment. SHR show genetically determined calcium homeostasis abnormality. Objective. To investigate protein metabolism disturbance and reveal the difference in the level of a major proteinkinase C substrate, NAP-22, between SHR and normotensive WKY strain. Design and methods. Our experiments were carried out on SHR and WKY rats. NAP-22 amount was examined in developing hippocampus and in parietal cortex by immunoblotting with anti-NAP-22 serum. Results. In all studied age groups (5-30 days), the amount of NAP-22 (including both aggregated and non-aggregated NAP-22 forms) in SHR telencephalon was considerably higher than in control WKY strain rats. There was also a significant difference between rate of development during considered period in SHR and WKY rats. Conclusion. Our results demonstrate that calcium homeostasis alterations could result in both cardiovascular abnormalities and in the damage of central nervous system through NAP-22 dysregulation.
About the Authors
O. S. Antonova
Pavlov Institute of Physiology of RAS, St Petersburg;
Institute for Analytical Instrumentation of RAS, St Petersburg
Russian Federation
Russian Federation
A. Y. Plekhanov
Petersburg Nuclear Physics Institute of RAS
Russian Federation
Russian Federation
E. I. Petrova
Pavlov Institute of Physiology of RAS, St Petersburg
Russian Federation
Russian Federation
S. Y. Reznik
Zoological Institute of RAS, St Petersburg
Russian Federation
Russian Federation
N. Z. Klyueva
Pavlov Institute of Physiology of RAS, St Petersburg
Russian Federation
Russian Federation
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Review
For citations:
Antonova O.S., Plekhanov A.Y., Petrova E.I., Reznik S.Y., Klyueva N.Z. Structural modifications of NAP-22 in the brain of spontaneously hypertensive rats. "Arterial’naya Gipertenziya" ("Arterial Hypertension"). 2011;17(4):342-346. (In Russ.) https://doi.org/10.18705/1607-419X-2011-17-4-342-346
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