Signaling Pathways Involved in NCAM-Induced Neurite Outgrowth

2009 ◽  
pp. 151-168 ◽  
Author(s):  
Dorte Kornerup Ditlevsen ◽  
Kateryna Kolkova
Keyword(s):  
Signaling Pathways ◽  
Neurite Outgrowth

scholarly journals The Insulin Receptor: A Potential Target of Amarogentin Isolated from Gentiana rigescens Franch That Induces Neurogenesis in PC12 Cells

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 581
Author(s):  
Lihong Cheng ◽  
Hiroyuki Osada ◽  
Tianyan Xing ◽  
Minoru Yoshida ◽  
Lan Xiang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Insulin Receptor ◽  
Signaling Pathways ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Mitogen Activated Protein Kinase ◽  
Potential Target ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Gentiana Rigescens

Amarogentin (AMA) is a secoiridoid glycoside isolated from the traditional Chinese medicine, Gentiana rigescens Franch. AMA exhibits nerve growth factor (NGF)-mimicking and NGF-enhancing activities in PC12 cells and in primary cortical neuron cells. In this study, a possible mechanism was found showing the remarkable induction of phosphorylation of the insulin receptor (INSR) and protein kinase B (AKT). The potential target of AMA was predicted by using a small-interfering RNA (siRNA) and the cellular thermal shift assay (CETSA). The AMA-induced neurite outgrowth was reduced by the siRNA against the INSR and the results of the CETSA suggested that the INSR showed a significant thermal stability-shifted effect upon AMA treatment. Other neurotrophic signaling pathways in PC12 cells were investigated using specific inhibitors, Western blotting and PC12(rasN17) and PC12(mtGAP) mutants. The inhibitors of the glucocorticoid receptor (GR), phospholipase C (PLC) and protein kinase C (PKC), Ras, Raf and mitogen-activated protein kinase (MEK) significantly reduced the neurite outgrowth induced by AMA in PC12 cells. Furthermore, the phosphorylation reactions of GR, PLC, PKC and an extracellular signal-regulated kinase (ERK) were significantly increased after inducing AMA and markedly decreased after treatment with the corresponding inhibitors. Collectively, these results suggested that AMA-induced neuritogenic activity in PC12 cells potentially depended on targeting the INSR and activating the downstream Ras/Raf/ERK and PI3K/AKT signaling pathways. In addition, the GR/PLC/PKC signaling pathway was found to be involved in the neurogenesis effect of AMA.

scholarly journals Different Outcomes of Unliganded and Liganded Estrogen Receptor-α on Neurite Outgrowth in PC12 Cells

Endocrinology ◽  
2008 ◽  
Vol 150 (1) ◽  
pp. 200-211 ◽  
Author(s):  
Yohann Mérot ◽  
François Ferrière ◽  
Luc Gailhouste ◽  
Guillaume Huet ◽  
Frédéric Percevault ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Estrogen Receptor Α ◽  
Akt Signaling ◽  
Induced Response ◽  
Nerve Growth

A precise description of the mechanisms by which estrogen receptor-α (ERα) exerts its influences on cellular growth and differentiation is still pending. Here, we report that the differentiation of PC12 cells is profoundly affected by ERα. Importantly, depending upon its binding to 17β-estradiol (17βE2), ERα is found to exert different effects on pathways involved in nerve growth factor (NGF) signaling. Indeed, upon its stable expression in PC12 cells, unliganded ERα is able to partially inhibit the neurite outgrowth induced by NGF. This process involves a repression of MAPK and phosphatidylinositol 3-kinase/Akt signaling pathways, which leads to a negative regulation of markers of neuronal differentiation such as VGF and NFLc. This repressive action of unliganded ERα is mediated by its D domain and does not involve its transactivation and DNA-binding domains, thereby suggesting that direct transcriptional activity of ERα is not required. In contrast with this repressive action occurring in the absence of 17βE2, the expression of ERα in PC12 cells allows 17βE2 to potentiate the NGF-induced neurite outgrowth. Importantly, 17βE2 has no impact on NGF-induced activity of MAPK and Akt signaling pathways. The mechanisms engaged by liganded ERα are thus unlikely to rely on an antagonism of the inhibition mediated by the unliganded ERα. Furthermore, 17βE2 enhances NGF-induced response of VGF and NFLc neuronal markers in PC12 clones expressing ERα. This stimulatory effect of 17βE2 requires the transactivation functions of ERα and its D domain, suggesting that an estrogen-responsive element-independent transcriptional mechanism is potentially relevant for the neuritogenic properties of 17βE2 in ERα-expressing PC12 cells. In the absence of its ligand, ERα partially inhibits the nerve growth factor-induced neurite outgrowth of PC12 cells, whereas, once liganded, it enhances differentiation.

Sez-6 May Play an Important Role in Neurite Outgrowth through the PKCgamma Signaling Pathways

2011 ◽  
Vol 66 ◽  
pp. 0614 ◽  
Author(s):  
J. Zhang ◽  
J. Zhang ◽  
Y. Wu ◽  
Y. Zhou ◽  
Z. Shao ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Neurite Outgrowth

Emodin induces neurite outgrowth through PI3K/Akt/GSK-3β-mediated signaling pathways in Neuro2a cells

2015 ◽  
Vol 588 ◽  
pp. 101-107 ◽  
Author(s):  
Shin-Ji Park ◽  
Mei Ling Jin ◽  
Hyun-Kyu An ◽  
Kyoung-Sook Kim ◽  
Min Jung Ko ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Neurite Outgrowth ◽  
Neuro2a Cells ◽  
Gsk 3Β

scholarly journals PPARγ and Cognitive Performance

2019 ◽  
Vol 20 (20) ◽  
pp. 5068 ◽  
Author(s):  
Michele d’Angelo ◽  
Vanessa Castelli ◽  
Mariano Catanesi ◽  
Andrea Antonosante ◽  
Reyes Dominguez-Benot ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neurodegenerative Diseases ◽  
Signaling Pathways ◽  
Neurite Outgrowth ◽  
Cognitive Performance ◽  
Nuclear Receptors ◽  
Neuroprotective Agents ◽  
Pathological Conditions ◽  
Pparγ Agonists ◽  
Mental Decline

Recent findings have led to the discovery of many signaling pathways that link nuclear receptors with human conditions, including mental decline and neurodegenerative diseases. PPARγ agonists have been indicated as neuroprotective agents, supporting synaptic plasticity and neurite outgrowth. For these reasons, many PPARγ ligands have been proposed for the improvement of cognitive performance in different pathological conditions. In this review, the research on this issue is extensively discussed.

Melanin-concentrating hormone induces neurite outgrowth in human neuroblastoma SH-SY5Y cells through p53 and MAPKinase signaling pathways

Peptides ◽  
2009 ◽  
Vol 30 (11) ◽  
pp. 2014-2024 ◽  
Author(s):  
Natacha Cotta-Grand ◽  
Carole Rovère ◽  
Alice Guyon ◽  
Alexandra Cervantes ◽  
Frédéric Brau ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Neurite Outgrowth ◽  
Human Neuroblastoma ◽  
Melanin Concentrating Hormone
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