scholarly journals Pro-apoptotic Bim Induction in Response to Nerve Growth Factor Deprivation Requires Simultaneous Activation of Three Different Death Signaling Pathways

2007 ◽  
Vol 282 (40) ◽  
pp. 29368-29374 ◽  
Author(s):  
Subhas C. Biswas ◽  
Yijie Shi ◽  
Andrew Sproul ◽  
Lloyd A. Greene
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Nerve Growth ◽  
Growth Factor Deprivation ◽  
Simultaneous Activation

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.

Effect of chronic autoimmune nerve growth factor deprivation on sympathetic neuroaxonal dystrophy in-rats

Synapse ◽  
1995 ◽  
Vol 20 (3) ◽  
pp. 249-256 ◽  
Author(s):  
Jo Anna Schroer ◽  
Lucie N. Beaudet ◽  
Robert E. Schmidt
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neuroaxonal Dystrophy ◽  
Nerve Growth ◽  
Growth Factor Deprivation

Nerve growth factor functions as a chemoattractant for mast cells through both mitogen-activated protein kinase and phosphatidylinositol 3-kinase signaling pathways

Blood ◽  
2000 ◽  
Vol 95 (6) ◽  
pp. 2052-2058 ◽  
Author(s):  
Junko Sawada ◽  
Atsuko Itakura ◽  
Akane Tanaka ◽  
Tohru Furusaka ◽  
Hiroshi Matsuda
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Mast Cells ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
Mitogen Activated Protein Kinase ◽  
Phosphatidylinositol 3 Kinase ◽  
Directional Migration ◽  
Nerve Growth ◽  
Mitogen Activated Protein

Abstract Despite being a well-characterized neurotrophic factor, nerve growth factor (NGF) influences survival, differentiation, and functions of mast cells. We investigated whether NGF was able to induce directional migration of rat peritoneal mast cells (PMCs). NGF clearly induced chemotactic movement of PMCs in a dose-dependent manner with the drastic morphological change and distribution of F-actin, which was completely blocked by pretreatment with Clostridium botulinumC2 toxin, an actin-polymerization inhibitor. Because PMCs constitutively express the NGF high-affinity receptor (TrkA) with a tyrosine kinase domain, we focused on downstream effectors in signaling cascades following the TrkA. NGF rapidly activated both mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K), and the addition of inhibitors specific for MAPK kinase and PI3K suppressed cell migration and these signals. In the coculture system with PMCs and fibroblasts, which produce biologically active NGF, directional migration of PMCs to fibroblasts was observed, and the addition of anti-NGF polyclonal antibodies significantly suppressed the migration of PMCs. These findings suggested that NGF initiated chemotactic movement of PMCs through both MAPK and PI3K signaling pathways following TrkA activation. Thus, locally produced NGF may play an important role in mast cell accumulation in allergic and nonallergic inflammatory conditions.

scholarly journals Nerve Growth Factor Stimulates Proliferation and Survival of Human Breast Cancer Cells through Two Distinct Signaling Pathways

2001 ◽  
Vol 276 (21) ◽  
pp. 17864-17870 ◽  
Author(s):  
Simon Descamps ◽  
Robert-Alain Toillon ◽  
Eric Adriaenssens ◽  
Valérie Pawlowski ◽  
Simon M. Cool ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Nerve Growth

scholarly journals Learning Impairment and Cholinergic Deafferentation after Cortical Nerve Growth Factor Deprivation

1997 ◽  
Vol 17 (10) ◽  
pp. 3796-3803 ◽  
Author(s):  
Humberto Gutiérrez ◽  
Marı́a Isabel Miranda ◽  
Federico Bermúdez-Rattoni
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
Growth Factor Deprivation ◽  
Learning Impairment

scholarly journals Effect of nerve growth factor on the proliferation in newborn bovine testicular Sertoli cells

Reproduction ◽  
2020 ◽  
Vol 160 (3) ◽  
pp. 405-415
Author(s):  
Qiaoge Niu ◽  
Maosheng Cao ◽  
Chenfeng Yuan ◽  
Yuwen Huang ◽  
Zijiao Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Male Reproduction ◽  
Nerve Growth ◽  
And Function

Nerve growth factor (NGF) has been proved to play important roles in male reproductive physiology, but the molecular mechanisms of NGF action remain unclear. In this study, the effects of NGF on the growth of newborn bovine testicular Sertoli (NBS) cells and the related signaling pathways were investigated. The NBS cells were treated in vitro with NGF (100 ng/mL) for 18 h. The expression levels of cell proliferation related genes, INHBB, and cytoplasmic specialization related gene were determined using real-time PCR and Western blot. The roles of PI3K/AKT and MAPK/ERK pathways in NGF-induced cell proliferation were investigated. It was found that NGF regulates proliferation and function of NBS cells via its receptor NTRK1 by activating the PI3K/ATK and MAPK/ERK signaling pathways. The study will help to further understand the role of NGF in male reproduction and provide new therapeutic targets for reproductive dysfunctions in male animals.

scholarly journals The Copper(II)-Assisted Connection between NGF and BDNF by Means of Nerve Growth Factor-Mimicking Short Peptides

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 301 ◽  
Author(s):  
Irina Naletova ◽  
Cristina Satriano ◽  
Adriana Pietropaolo ◽  
Fiorenza Gianì ◽  
Giuseppe Pandini ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Noncovalent Interactions ◽  
Critical Role ◽  
Camp Response Element Binding ◽  
Copper Binding ◽  
Bdnf Expression ◽  
Bdnf Mrna ◽  
Nerve Growth

Nerve growth factor (NGF) is a protein necessary for development and maintenance of the sympathetic and sensory nervous systems. We have previously shown that the NGF N-terminus peptide NGF(1-14) is sufficient to activate TrkA signaling pathways essential for neuronal survival and to induce an increase in brain-derived neurotrophic factor (BDNF) expression. Cu2+ ions played a critical role in the modulation of the biological activity of NGF(1-14). Using computational, spectroscopic, and biochemical techniques, here we report on the ability of a newly synthesized peptide named d-NGF(1-15), which is the dimeric form of NGF(1-14), to interact with TrkA. We found that d-NGF(1-15) interacts with the TrkA-D5 domain and induces the activation of its signaling pathways. Copper binding to d-NGF(1-15) stabilizes the secondary structure of the peptides, suggesting a strengthening of the noncovalent interactions that allow for the molecular recognition of D5 domain of TrkA and the activation of the signaling pathways. Intriguingly, the signaling cascade induced by the NGF peptides ultimately involves cAMP response element-binding protein (CREB) activation and an increase in BDNF protein level, in keeping with our previous result showing an increase of BDNF mRNA. All these promising connections can pave the way for developing interesting novel drugs for neurodegenerative diseases.

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