- 作者: Philip K. Liu
- 作者服務機構: Departimnts of Neurosurgery and Molecular and Cell Biology and Cardiovascular Disease Program of the Department of Medicine, Baylor College of Medicine
- 中文摘要: --
- 英文摘要: Diseases of the heart are the No.1 killer in industrializedcountries.Brain injury can develop as a result of cerebralischemia-reperfusion due to stroke(brain attack) andother cardiovascular diseases. Learning about the dis-ease is the best way to reduce disability and death.Wepresent here whether gene repair activities are associat-ed with neuronal death in an ischemia-reperfusion mod-el that simulates stroke in male Long-Evans rats. Thisexperimental stroke model is known to induce necrosisin the ischemic cortex. Cerebra∣ischemia causes overac-tivation of membrane receptors and accumulation ofextracellur glutamate and intracellular calcium,whichactivates neuronal nitric oxide synthase, causing dam-age to lipids, proteins, and nucleic acids, and reducesenergy sources with consequent functional deteriora-tion,leading to cell death.Restoration processes normal-.ly repair genes with few errors. However, ischemia ele-vates oxidative DNA lesions despite these repair mecha-nisms.These episodes concurrently occur with the in-duction of immediate-early genes that critically activateother late genes in the signal transduction pathway.Damage, repair, and transcription of the c-fos gene arepresented here as examples, because Fos peptide, oneof the components of activator protein 1,activates nervegrowth factor and repair mechanisms. The results of ourstudies show that treatments with 7-nitroindazole, a spe-cific inhibitor of nitric oxide synthase known to attenuatenitric oxide, oxidative DNA lesions, and necrosis, in-crease intact c-fos mRNA levels after stroke.This sug-gests that the accuracy of gene expression could beaccounted for the recovery of cellular function after cere-brat injury.
- 中文關鍵字: --
- 英文關鍵字: Gene repair. Head injury. Immediate-early genes. Mutagenesis. Neuroregeneration. Oxidative Stress. Plasticity. Signal transduction. Stroke. Transcription