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Increased calpain expression following experimental cerebral venous thrombosis in rats
Martin Liebetrau1, Dusica Gabriejcic-Geiger, Phillip Meyer
1Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians University, Marchioninistr. 15, Munich 81377, Germany.
Introduction:
Calpains are intracellular proteases that are activated by increased intracellular calcium with proteolytic activity mainly against the cytoskeleton. We tested the expression of calpains and their substrates in an animal model of experimental cerebral venous thrombosis.
Materials And Methods:
Cerebral venous thrombosis was induced in seven male rats by rostral and caudal ligation of the superior sagittal sinus and injection of a thrombogenic cephalin suspension. Each animal survived 3 h of thrombosis. Using a polyclonal antibody against the 80 kD subunit of micro-calpain, immunohistochemistry of the region of interest (venous infarction) showed a loss of microtubule-associated protein-2. The micro-calpain-positive cells in the region of interest and normal tissue were measured using a video-imaging microscopy unit with magnification power of 400x. A cell was considered calpain positive when the nucleus and the periplasma were stained by the micro-calpain antibody.
Results:
The mean infarct size was 13.4+/-3.7% of one whole coronal section. A total of 57+/-14% of the cells were found to be calpain positive in the region of interest, whereas 5+/-2% of all cellular elements in unaffected tissue were calpain positive (p<0.001).
Conclusions:
In conclusion, cerebral venous thrombosis causes an increase in calpain expression in affected tissue which is manifested by a loss of microtubule-associated protein-2. This increase might mediate secondary neuronal injury.
