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首页> 外文期刊>Progress in brain research >Pathways of survival induced by NGF and extracellular ATP after growth factor deprivation.
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Pathways of survival induced by NGF and extracellular ATP after growth factor deprivation.

机译：生长因子剥夺后，NGF和细胞外ATP诱导的生存途径。

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摘要

In a previous work we demonstrated that extracellular adenosine-5'-triphosphate (ATP), acting on P2 receptors, exerts neuritogenic and trophic effects on the phaeochromocytoma PC12 cell line. These actions are comparable to those sustained by nerve growth factor (NGF) and involve several overlapping pathways. In this work, we describe some of the mechanisms recruited by ATP and NGF in maintaining PC12 cell survival after serum deprivation. We show that both ATP and NGF upregulate the expression of the stress-induced heat shock protein HSP70 and HSP90, whilst glucose-response protein GRP75 and GRP78 are not affected. In parallel with NGF, ATP prevents the cleavage and activation of caspase-2 and inhibits the release of cytochrome c from mitochondria into the cytoplasm. Finally, neither NGF, nor ATP directly modulate the expression of P2 receptors in the induction of cell survival. Our data contribute to dissect the biological mechanisms activated by extracellular purines exerting trophic actions and to establish that survival and neurite outgrowth lie on different mechanistic pathways.
机译：在以前的工作中，我们证明了作用于P2受体的细胞外5'-三磷酸腺苷（ATP）对嗜铬细胞瘤PC12细胞系产生神经毒性和营养作用。这些作用与神经生长因子（NGF）维持的作用相当，并且涉及几种重叠的途径。在这项工作中，我们描述了由ATP和NGF召集的维持血清剥夺后维持PC12细胞存活的一些机制。我们表明，ATP和NGF都上调了应激诱导的热休克蛋白HSP70和HSP90的表达，而葡萄糖响应蛋白GRP75和GRP78却没有受到影响。 ATP与NGF并行，可阻止caspase-2的裂解和活化，并抑制细胞色素c从线粒体释放到细胞质中。最后，在诱导细胞存活中，NGF和ATP均未直接调节P2受体的表达。我们的数据有助于剖析胞外嘌呤发挥营养作用激活的生物学机制，并确定存活和神经突生长位于不同的机制途径上。

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