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Induction of plasminogen in rat hippocampal pyramidal neurons by kainic acid.

机译:红藻氨酸对大鼠海马锥体神经元纤溶酶原的诱导作用。

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摘要

Tissue plasminogen activator (tPA) is used to treat acute stroke, but tPA- and plasminogen-gene-deficient mice exhibit resistance to neurodegeneration. Thus, it is unclear whether the tPA-plasminogen system, an extracellular proteolytic cascade plays a helpful or harmful role, and whether plasminogen is induced by neurodegeneration. In the CA3, kainic acid (KA)-injection caused neuronal damage after 6 h, and almost all of the neurons were lost after 7 days. Plasminogen mRNA was strongly induced 6 h after injection, then gradually decreased, and was very weak at 2 days after injection. Plasminogen protein was expressed after 6 h and localized in abnormally shaped neurons. The in vivo expression of plasminogen was synchronous with morphological changes in neurons. These results suggest that the expression of plasminogen induced by KA-injection may disrupt of neuron-extracellular matrix interaction and thereby contribute to cell death in neurons in the hippocampus.
机译:组织纤溶酶原激活物(tPA)用于治疗急性中风,但tPA和纤溶酶原基因缺陷的小鼠表现出对神经变性的抵抗力。因此,尚不清楚tPA-纤溶酶原系统,细胞外蛋白水解级联反应是起辅助作用还是有害作用,以及纤溶酶原是否由神经退行性变所诱导。在CA3中,注射海藻酸(KA)会在6 h后引起神经元损伤,并且在7天后几乎所有神经元都丢失。注射后6小时,纤溶酶原mRNA被强烈诱导,然后逐渐降低,并在注射后2天非常弱。纤溶酶原蛋白在6 h后表达,并定位于异常形状的神经元中。纤溶酶原的体内表达与神经元的形态变化同步。这些结果表明,KA注射诱导的纤溶酶原的表达可能破坏神经元与细胞外基质的相互作用,从而导致海马神经元细胞死亡。

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