Regeneration of injured axons with oligodendrocytic signal-processing systems as a marker

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We have studied mRNA and protein expression of myelencephalon-specific protease (MSP) in the brain ischemia and brain injury model in rats, because MSP is oligodendrocyte-specific serine protease and MSP expression is relating to axonal regeneration. As a result, we have detected MSP mRNA and protein expression in the oligodendrocytes locating at peri-ischemic area 3 to 7 days after cerebral ischemia. Question then arises whether MSP expression is caused by direct ischemic injury to the peri-ischemic oligodendrocytes or indirect effect of edema fluid formation on oligodendrocytes. To answer this question, we developed cold injury model in which edema developed around lesion but ischemic injury to the oligodendrocyte was not occurring. We detected in the cold injury model that MSP expression occurred on the 5^<th> day after cold injury. With this result we concluded that edema fluid extending to the surrounding lesion might activate oligodendrocytes and express MSP mRNA and protein expression. We did double immunostaining of MSP and oligodendrocyte-specific marker CNPase, and identified that both markers were co-localizing in the same oligodendrocyte. The results suggest that edema fluid activates oligodendrocytes and act for regeneration of axons. We also did Western blotting of the MSP and identified that MSP proteins has bands at 19kDa (authentic MSP protein) and 37, 40 and 50kDa's. The 37kDa bands increased its volume at 6 hours and 5-7days after cold injury. Those two peaks of reactive production suggested two mechanism of oligodendrocytes activation, initial direct stimulation through neuronal network and secondary indirect stimulation through edema fluid extension. That similar result was also identified in the subarachnoid hemorrhage model and intracerebral hemorrhage model.