2003Acta Universitatis Medicinalis Secondae ShanghaiRequires access

Expression of Amyloid Precursor Protein Genes following Focal Cerebral Ischemia and Reperfusion in Rats

Dai Qin-shun

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Abstract

Objective To elucidate amyloid precursor protein ( APP) gene expression in cerebral cortex following cerebral ischemia -reperfusion injuries. Methods Rats(n=136) were given an is-chemic insult through unilateral MCA occlusion and reperfusion by use of intralurainal suture, which was composed of 1 hour's occlusion and reperfusion for Oh, Ih, 3h, 8h, 1d, 3d, 7d, respectively. The rats were sacrificed and cerebral cortex was dissected. The mRNA levels of APP770,751,695 was investigated by RT - PCR. Also neuronal damage and glial fibrillary acidic protein immunohistochemistry were histologi-cally examined. Results After transient ischemia, the Kunitz protease inhibitor - bearing isoforms(KPI -APP) were increased whereas APP695 which lack KPI domain was decreased. Neuronal damage and GFAP immunoreactive astrocytes were also observed. Conclusion The results indicate that focal transient ischemia alters KPI - APP/APP695 ratio in cerebral cortex and this shift in APP isoforms could be related to neurodegeneration and /or activation of astrocytes during the ischemic process.

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Objective To elucidate amyloid precursor protein ( APP) gene expression in cerebral cortex following cerebral ischemia -reperfusion injuries. Methods Rats(n=136) were given an is-chemic insult through unilateral MCA occlusion and reperfusion by use of intralurainal suture, which was composed of 1 hour's occlusion and reperfusion for Oh, Ih, 3h, 8h, 1d, 3d, 7d, respectively. The rats were sacrificed and cerebral cortex was dissected. The mRNA levels of APP770,751,695 was investigated by RT - PCR. Also neuronal damage and glial fibrillary acidic protein immunohistochemistry were histologi-cally examined. Results After transient ischemia, the Kunitz protease inhibitor - bearing isoforms(KPI -APP) were increased whereas APP695 which lack KPI domain was decreased. Neuronal damage and GFAP immunoreactive astrocytes were also observed. Conclusion The results indicate that focal transient ischemia alters KPI - APP/APP695 ratio in cerebral cortex and this shift in APP isoforms could be related to neurodegeneration and /or activation of astrocytes during the ischemic process.

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Available abstract

Objective To elucidate amyloid precursor protein ( APP) gene expression in cerebral cortex following cerebral ischemia -reperfusion injuries. Methods Rats(n=136) were given an is-chemic insult through unilateral MCA occlusion and reperfusion by use of intralurainal suture, which was composed of 1 hour's occlusion and reperfusion for Oh, Ih, 3h, 8h, 1d, 3d, 7d, respectively. The rats were sacrificed and cerebral cortex was dissected. The mRNA levels of APP770,751,695 was investigated by RT - PCR. Also neuronal damage and glial fibrillary acidic protein immunohistochemistry were histologi-cally examined. Results After transient ischemia, the Kunitz protease inhibitor - bearing isoforms(KPI -APP) were increased whereas APP695 which lack KPI domain was decreased. Neuronal damage and GFAP immunoreactive astrocytes were also observed. Conclusion The results indicate that focal transient ischemia alters KPI - APP/APP695 ratio in cerebral cortex and this shift in APP isoforms could be related to neurodegeneration and /or activation of astrocytes during the ischemic process.

Key concepts: Ischemia, Glial fibrillary acidic protein, Cerebral cortex, Gene isoform, Neurodegeneration, Amyloid precursor protein, Cortex (anatomy), Middle cerebral artery

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Expression of Amyloid Precursor Protein Genes following Focal Cerebral Ischemia and Reperfusion in Rats — Research Paper | ScholarLens