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神经生长因子诱导PC12细胞中的神经突形成与内源性细胞神经节苷脂无关。

Nerve growth factor-induced neurite formation in PC12 cells is independent of endogenous cellular gangliosides.

作者信息

Li R, Kong Y, Ladisch S

机构信息

Glycobiology Program, Center for Cancer and Transplantation Biology, Children's Research Institute, The George Washington University School of Medicine, Washington, DC 20010, USA.

出版信息

Glycobiology. 1998 Jun;8(6):597-603. doi: 10.1093/glycob/8.6.597.

Abstract

The PC12 rat pheochromocytoma cell line is an established model for nerve growth factor (NGF)-induced neurite formation. It has been shown that when gangliosides are added to the culture medium of PC12 cells, NGF-induced neurite formation of PC12 cells is enhanced. To determine the role of endogenous cellular gangliosides themselves in NGF-elicited neurite formation, we depleted cellular gangliosides using the new specific glucosylceramide synthase inhibitor, d, l-threo-1-phenyl-2-hexadecanoylamino-3-pyrrolidino-1-propanol.HCl (PPPP). 0.5-2 microM PPPP rapidly inhibited ganglioside synthesis and depletedcellular gangliosides. Nonetheless, over a concentration range of 5-100 ng/ml NGF, in both low serum and serum-free medium, neurite formation was normal. Even pretreatment of PC12 cells for up to 6 days with 1 microM PPPP followed by cotreatment with PPPP and NGF for 10 days, still did not inhibit neurite formation. The conclusion that ganglioside depletion did not block neurite formation stimulated by NGF was supported by the lack of effect of PPPP, under these same conditions, on cellular acetylcholine esterase activity, a neuronal differentiation marker (73.8 +/- 12.1 versus 67.2 +/- 4.6 nmol/min/mg protein at 50 ng/ml NGF; control versus 1 microM PPPP). These findings, together with previous studies showing enhancement of NGF-induced neurite formation by exogenous gangliosides, underscore the vastly different effects that exogenous gangliosides and endogenous gangliosides may have upon cellular functions.

摘要

PC12大鼠嗜铬细胞瘤细胞系是神经生长因子(NGF)诱导神经突形成的既定模型。研究表明,当将神经节苷脂添加到PC12细胞的培养基中时,NGF诱导的PC12细胞神经突形成会增强。为了确定内源性细胞神经节苷脂自身在NGF引发的神经突形成中的作用,我们使用新型特异性葡糖神经酰胺合酶抑制剂d,l-苏式-1-苯基-2-十六烷酰氨基-3-吡咯烷基-1-丙醇盐酸盐(PPPP)来消耗细胞神经节苷脂。0.5 - 2 microM的PPPP能迅速抑制神经节苷脂的合成并耗尽细胞神经节苷脂。然而,在5 - 100 ng/ml NGF的浓度范围内,无论是在低血清还是无血清培养基中,神经突形成都是正常的。即使先用1 microM的PPPP预处理PC12细胞长达6天,然后再将其与PPPP和NGF共同处理10天,仍不会抑制神经突形成。在相同条件下,PPPP对细胞乙酰胆碱酯酶活性(一种神经元分化标志物)没有影响,这支持了神经节苷脂消耗不会阻断NGF刺激的神经突形成这一结论(在50 ng/ml NGF时,对照组细胞乙酰胆碱酯酶活性为73.8±12.1 nmol/min/mg蛋白,1 microM PPPP处理组为67.2±4.6 nmol/min/mg蛋白)。这些发现,连同之前显示外源性神经节苷脂增强NGF诱导的神经突形成的研究,强调了外源性神经节苷脂和内源性神经节苷脂对细胞功能可能产生的巨大不同影响。

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