scholarly journals Botanical Drug Puerarin Coordinates with Nerve Growth Factor in the Regulation of Neuronal Survival and Neuritogenesis via Activating ERK1/2 and PI3K/Akt Signaling Pathways in the Neurite Extension Process

2014 ◽  
Vol 21 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Jia Zhao ◽  
Yuan-Yuan Cheng ◽  
Wen Fan ◽  
Chuan-Bin Yang ◽  
Shui-Fen Ye ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Neuronal Survival ◽  
Akt Signaling ◽  
Nerve Growth ◽  
Neurite Extension ◽  
Botanical Drug ◽  
Extension Process

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.

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
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