Expressions of neuropilin-1, neuropilin-2 and semaphorin 3A mRNA in the rat brain after middle cerebral artery occlusion

This study investigated the spatial and temporal expressions of mRNA encodi ng neuropilin (Npn)-1, Npn-2 and semaphorin3A (Sema3A) in the rat brain aft er occlusion of the middle cerebral artery (MAC) distal to the striate bran ches. The expression of Npn-1 mRNA was transiently upregulated in layers V and VI of the parietal cortex not entering infarction on the lesion side fr om 3 to 6 h after MCA occlusion. The transient up-regulation of Npn-1 mRNA expression was presumably accompanied by an increase in Npn-1 protein as sh own by immunohistochemistry in combination with in situ hybridization histo chemistry. Intense Npn-2 mRNA expression was noted temporarily in layer II of the parietal cortex on the lesion side from I to 6 h after MCA occlusion . The expression of Sema3A mRNA was upregulated in layer VI of the non-infa rcted parietal cortex on the lesion side at 6 h after MCA occlusion. The ab ove increases in mRNA expression were no longer observed at 12 h after MCA occlusion. The expressions of Npn-1, -2 and Sema3A mRNA were not detected i n the ventroposterior thalamic nucleus undergoing secondary degeneration af ter MCA occlusion. In the infarct lesion or ischemic core, neuronal express ions of Npn-1, -2 and Sema3A disappeared by 3 days after MCA occlusion as t he neurons in situ entered apoptosis or necrosis. In contrast, ED-1-positiv e microglia/macrophages with Npn-l and Npn-2 mRNA were observed in the infa rct lesion at I week after MCA occlusion. These findings suggest that the t emporal up-regulation of Npn-l and Sema 3A mRNA expressions in the non-infa rcted parietal cortex on the lesion side is insufficient to induce neuronal cell death possibly because the up-regulated mRNA molecules are not fully translated and that the overexpression. of Npn-1 and/or Npn-2 in the ischem ic core with degenerating neurons enables activated microglial cells to con tact the damaged neurons in situ for phagocytosis. (C) 2001 Elsevier Scienc e BY A-H rights reserved.