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首页> 外文期刊>Journal of Cellular Physiology >The role of nerve growth factor in hyperosmolar stress induced apoptosis.
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The role of nerve growth factor in hyperosmolar stress induced apoptosis.

机译：在hyperosmolar神经生长因子的作用应力诱导细胞凋亡。

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摘要

Nerve growth factor (NGF) is a neurotrophic factor that plays an important role in the differentiation and growth of neuronal cells. It is also regarded as an inflammatory mediator in non-neuronal tissues under physiological stress conditions. The mechanisms of NGF production and its roles in hyperosmolar stress conditions have not been established. In this study, we show that NGF levels in cultured human corneal epithelial cells (HCECs) were up-regulated during hyperosmolar stress by IL-1beta, but not TNF-alpha. NF-kappaB activity, but not AP-1, increased significantly under hyperosmolar conditions, and NF-kappaB was involved in IL-1beta-induced NGF production. IL-1beta-induced NGF production reduced JNK phosphorylation and HCEC apoptosis. These changes were accompanied by down-regulated Bax and caspase-3, -8, -9 activities. NGF siRNA and the tyrosine kinase inhibitor K252a significantly enhanced Bax up-regulation. Thus, up-regulated NGF under hyperosmolar stress conditions may contribute, at least inpart, to reduced HCEC apoptosis. This conclusion suggests that enhanced NGF expression may be beneficial in recovering corneal damage due to chronic hyperosmolar stress.
机译：神经生长因子(神经生长因子)是一种神经营养因子中起着重要的作用神经细胞的分化和生长。也被认为是炎症介质在吗non-neuronal组织生理压力之下条件。这两个角色在hyperosmolar压力条件没有建立。人工培养的角膜上皮神经生长因子水平细胞(HCECs)期间被上调由IL-1beta hyperosmolar压力,但不是tnf。hyperosmolar下显著增加条件,NF-kappaB参与IL-1beta-induced神经生长因子的生产。神经生长因子减少物磷酸化和生产HCEC细胞凋亡。理气伯灵顿和caspase-3 8 9活动。抑制剂K252a显著增强的伯灵顿老年病。可能造成hyperosmolar应力条件,至少这部分,HCEC细胞凋亡减少。结论表明,增强神经生长因子表达可能有利于恢复角膜损伤由于慢性hyperosmolar压力。

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