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首页> 外文期刊>Molecular biology of the cell >The hippocampal laminin matrix is dynamic and critical for neuronal survival
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The hippocampal laminin matrix is dynamic and critical for neuronal survival

机译：海马层粘连蛋白基质是动态的，对神经元存活至关重要

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摘要

Laminins are extracellular matrix proteins that participate in neuronal development, survival, and regeneration. During excitotoxin challenge in the mouse hippocampus, neuron interaction with laminin-10 (alpha5,beta1,gamma1) protects against neuronal death. To investigate how laminin is involved in neuronal viability, we infused laminin-1 (alpha1,beta1,gamma1) into the mouse hippocampus. This infusion specifically disrupted the endogenous laminin layer. This disruption was at least partially due to the interaction of the laminin-1 gamma1 chain with endogenous laminin-10, because infusion of anti-laminin gamma1 antibody had the same effect. The disruption of the laminin layer by laminin-1 1) did not require the intact protein because infusion of plasmin-digested laminin-1 gave similar results; 2) was posttranscriptional, because there was no effect on laminin mRNA expression; and 3) occurred in both tPA(-/-) and plasminogen(-/-) mice, indicating that increased plasmin activity was not responsible. Finally, although tPA(-/-) mice are normally resistant to excitotoxin-induced neurodegeneration, disruption of the endogenous laminin layer by laminin-1 or anti-laminin gamma1 antibody renders the tPA(-/-) hippocampal neurons sensitive to kainate. These results demonstrate that neuron interactions with the deposited matrix are not necessarily recapitulated by interactions with soluble components and that the laminin matrix is a dynamic structure amenable to modification by exogenous molecules. [References: 52]
机译：层粘连蛋白是参与神经元发育，存活和再生的细胞外基质蛋白。在小鼠海马中激发毒素攻击期间，与层粘连蛋白10（alpha5，beta1，gamma1）的神经元相互作用可以防止神经元死亡。为了研究层粘连蛋白如何参与神经元生存能力，我们向小鼠海马中注入了层粘连蛋白-1（alpha1，beta1，gamma1）。这种输注特别破坏了内源性层粘连蛋白层。这种破坏至少部分是由于层粘连蛋白-1 gamma1链与内源性层粘连蛋白10的相互作用，因为输注抗层粘连蛋白gamma1抗体具有相同的作用。层粘连蛋白-1破坏层粘连蛋白层1）不需要完整蛋白，因为输注纤溶酶消化的层粘连蛋白-1产生相似的结果。 2）是转录后的，因为对层粘连蛋白mRNA表达没有影响;和3）都发生在tPA（-/-）和纤溶酶原（-/-）小鼠中，表明纤溶酶活性的升高不是原因。最后，尽管tPA（-/-）小鼠通常对兴奋性毒素诱导的神经变性具有抗性，但层粘连蛋白-1或抗层粘连蛋白γ1抗体破坏内源性层粘连蛋白层使tPA（-/-）海马神经元对红藻氨酸盐敏感。这些结果表明，与沉积的基质的神经元相互作用不一定通过与可溶性组分的相互作用来概括，并且层粘连蛋白基质是易于被外源分子修饰的动态结构。 [参考：52]

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