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

نویسندگان

  • R Li
  • Y Kong
  • S Ladisch
چکیده

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.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Human Olfactory Ecto-mesenchymal Stem Cells Displaying Schwann-Cell-Like Phenotypes and Promoting Neurite Outgrowth in Vitro

Strategies of Schwann cell (SC) transplantation to regenerate the peripheral nerve injury involves many limitations. Stem cells can be used as alternative cell sources for differentiation into SCs. Given the high potential of neural crest-derived stem cells for the generation of multiple cell lineages, in this research, we considered whether olfactory ecto-mesenchymal stem cells (OE-MSCs) derive...

متن کامل

Modulation of H2O2- Induced Neurite Outgrowth Impairment and Apoptosis in PC12 Cells by a 1,2,4-Triazine Derivative

Introduction: Increased oxidative stress is widely accepted to be a factor in the development and progression of Alzheimer’s disease. Triazine derivatives possess a wide range of pharmacological activities including anti-oxidative and anti-in.ammatory actions. In this study, we aimed to investigate the possible protective effect of 3-thioethyl-5,6-dimethoxyphenyl-1,2,4-triazine (TEDMT) on H2O2-...

متن کامل

Neurotrophin Promotes Neurite Outgrowth by Inhibiting Rif GTPase Activation Downstream of MAPKs and PI3K Signaling

Members of the well-known semaphorin family of proteins can induce both repulsive and attractive signaling in neural network formation and their cytoskeletal effects are mediated in part by small guanosine 5'-triphosphatase (GTPases). The aim of this study was to investigate the cellular role of Rif GTPase in the neurotrophin-induced neurite outgrowth. By using PC12 cells which are known to cea...

متن کامل

SH2B1beta enhances fibroblast growth factor 1 (FGF1)-induced neurite outgrowth through MEK-ERK1/2-STAT3-Egr1 pathway.

Genetic studies have established the crucial roles of FGF signaling, FGF-induced gene expression and morphogenesis during embryogenesis. In this study, we showed that overexpressing a signaling adaptor protein, SH2B1beta, enhanced FGF1-induced neurite outgrowth in PC12 cells. SH2B1beta has previously been shown to promote nerve growth factor (NGF) and glial cell line-derived neurotrophic factor...

متن کامل

Dependence of neurotrophic factor activation of Trk tyrosine kinase receptors on cellular sialidase.

A direct link between receptor glycosylation and activation following natural ligand interaction has not been observed. Here, we discover a membrane sialidase-controlling mechanism that depends on ligand binding to its receptor to induce enzyme activity which targets and desialylates the receptor and, consequently, causes the induction of receptor dimerization and activation. We also identify a...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Glycobiology

دوره 8 6  شماره 

صفحات  -

تاریخ انتشار 1998