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纤丝状Aβ_(42)对GSK-3β和PP2A Cα表达的影响

Effects of fibrillar Aβ(42) on expressions of GSK-3β and PP2A Cα
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摘要 目的 探讨纤丝状Aβ^(42)对GSK-3β和PP2A Cα表达的影响。方法 应用立体定向技术对15月龄雄性SD大鼠进行海马内注射纤丝状Aβ^(42)或双蒸水,采用免疫组织化学染色方法,观察海马神经元GSK-3β和PP2A Cα的表达改变,并进行图像分析。结果 AB_(42)组海马神经元GSK-3β的表达明显高于双蒸水组,但两组的海马神经元PP2A Cα的表达没有明显差异。结论 纤丝状Aβ_(42)能使海马神经元GSK-3β表达上调,而对PP2A Cα的表达没有明显影响,提示纤丝状Aβ_(42)诱导tau蛋白过度磷酸化可能与GSK-3β表达上调有关。 Objective To explore the effects of fibrillar amyloid-beta peptide-42 (Aβ_(42)) on expressions of glycogen synthase kinase-3 (GSK-3β) and phosphatase 2A (PP2A) Ca. Methods Stereotaxic intrahippocampal microinjections of fibrillar Aβ_(42)or double-distilled water (ddH20) into 15-month SD male rats were performed and the expressions of GSK-3β and PP2A Cα in hippocampal neurons were observed immunohistochemically. Results The expressions of GSK-3β in the hippocampal neurons of fibrillar Aβ_(42) group were significantly stronger than those of ddH_2O group. However, the expressions of PP2A Cα in hippocampal neurons of both groups were of no significant difference. Conclusion Fibrillar Aβ_(42) induced higher expression of GSK-3β but had no significant effect on the expression of PP2A Cα in hippocampal neurons, It suggests that hyperphosphorylation of tau protein induced by fibril lar Aβ_(42) may contribute to the higher expression of GSK-3β.
出处 《中华神经医学杂志》 CAS CSCD 2004年第4期248-250,共3页 Chinese Journal of Neuromedicine
基金 广州市科委科技项目基金(JB02 2000-2-026-01)
关键词 纤丝状Aβ42 Β-淀粉样肽 糖原合成酶激酶-3Β 蛋白磷酸酯酶2A TAU蛋白 磷酸化过度 Aβ_(42) GSK-3β PP2A tau protein hyperphosphorylation
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  • 1申洪.免疫组织化学染色定量方法研究(Ⅲ)[J].中国组织化学与细胞化学杂志,1995,4(1):89-92. 被引量:401
  • 2申洪,陆药丹.免疫组织化学染色的定量方法研究[J].生物医学工程学杂志,1993,10(4):281-284. 被引量:127
  • 3包新民 舒斯云 主编.大鼠脑立体定向图谱第1版[M].北京:人民卫生出版社,1991.47-50.
  • 4Maho MK, Masato H, Koji T, et al. Hyperphosphorylation of tau in PHF. Nuerobiol of Aging, 1995, 16(3): 365.
  • 5Arriagada PV, Growdon JH, Hedley-Whyte T, et al. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease. Neurology, 1992, 42(3): 631.
  • 6Busciglio J, Lorenzo A, Yeh J, et al. β-Amyloid fibrils induce tau phosphorylation and loss of microtubule binding. Neuron, 1995, 14(4) :879.
  • 7Davis DR, Brion JP, Couck AM, et al. The phosphorylation state of the microtubule-associated protein tau as affected by glulamate, colchicine and β-amyloid in primary rat cortical neuronal cultures. Biochem. J,1995, 309(4): 941.
  • 8Wolozin B, Behl C. Mechanisms of neurodegenerative disorders: part 1 :protein aggregates. Arch Neurol, 2000, 57(6) : 793.
  • 9Lorenzo A, Yankner BA. β-amyloid neurotoxity requires fibril formation and is inhibited by Congo red. Proc Natl Acad Sci USAf, 1994, 91(25) :12243.
  • 10申洪.免疫组织化学显色反应强度定量方法研究(Ⅱ)[J].细胞与分子免疫学杂志,1994,11(4):33-35. 被引量:52

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