Neuronal ERCC6 mRNA expression in rat brain induced by a transient focal cerebral ischemia

AIM: To study whether the excision repair cross-complementing group 6 (ERCC 6) is involved in the neuronal pathophysiological process following cerebra l ischemia-reperfusion injury. METHODS: A transient middle cerebral artery occlusion (MCAO) was used to induce cerebral ischemia-reperfusion injury in rat brain. Northern blot was used to check a specific signal for oligonucl eotide probe. The expression of ERCC6 mRNA in the rat brain was observed by in situ hybridization. The specific cellular distribution of ERCC6 mRNA in the neuron or glia of the rat brain was analyzed by double staining combin ed with confocal laser scanning microscopic analysis. RESULT: The expressio n of ERCC6 mRNA in the penumbra area increased following ischemia and reper fusion with a time-dependent manner. ERCC6 was expressed on d 2, reached pe ak values on d 3, and kept high level even on d 14 of reperfusion following ischemia. Number of ERCC6 mRNA expressive cell in the penumbra area on d I , d 2, d 3, d 7, d 14 of reperfusion following ischemia were (Olt 0), (253 +/- 56), (816 +/- 355), (341 +/- 185), (128 +/- 95) x 10(6) cells/m(2), res pectively. Confocal microscopic analysis showed that ERCC6 mRNA coexpressed with phosphopyruvate hydratase in the neurons and with glial fibrillary ac idic protein (GFAP) in a few proliferation astrocyte glia. CONCLUSION: The expression of transcription-repair coupling factor ERCC6 mRNA in the neuron and glia was induced by ischemia-reperfusion injury.