Multiple agents rescue PC12 cells from serum-free cell death by translation- and transcription-independent mechanisms
TL;DR: Findings indicate that survival was promoted by mechanisms that do not require synthesis of RNA or protein, and Regulation of protein kinase activity appears to be a common feature of each pathway and may play a key convergent role in mediating prevention of cell death.
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Abstract: Past studies revealed that NGF and fibroblast growth factor (FGF) prevent the death of PC 12 pheochromocytoma cells that otherwise occurs in serum-free medium. Additional agents were tested here for their abilities to promote long-term survival of naive and NGF-pretreated (primed) PC 12 cells in serum-free conditions. Forskolin and permeant cAMP analogs effectively prevented serum-free cell death, as did micromolar levels of insulin and 10-100-nM levels of insulin-like growth factors I and II. In contrast to NGF and FGF, none of these agents caused neuronal differentiation of naive cells or neurite regeneration by primed cells. Each of the agents also prevented rapid cell death in a balanced salt solution, thus apparently ruling out a mechanism dependent on regulation of nutrient uptake. Epidermal growth factor and elevated K+ appeared to slow the rate of cell death, but did not promote long-term survival; phorbol ester, dexamethasone, or vanadate did not prevent cell death. Each of the survival-promoting agents was effective even when macromolecular synthesis was blocked. Because the synthesis inhibitors themselves did not significantly prevent cell death, such findings indicate that survival was promoted by mechanisms that do not require synthesis of RNA or protein. In addition, various lines of experimental evidence (using the kinase inhibitor K-252a or PC 12 cell variants deficient either in protein kinase A activity or in responsiveness to NGF) further suggested that the effective agents maintain survival by independent initial pathways. Regulation of protein kinase activity appears to be a common feature of each pathway and may therefore play a key convergent role in mediating prevention of cell death.
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•Journal Article
Apoptosis induced by serum deprivation of PC12 cells is not preceded by growth arrest and can occur at each phase of the cell cycle.
TL;DR: The results show that cells from all phases of the cell cycle are damaged upon serum deprivation and thus suggest that the apoptotic cell death of nonsynchronized PC12 cells may occur from each phase of thecell cycle.
Promotion of Neuronal Survival by GM1 Ganglioside: Phenomenology and Mechanism of Action
Giovanna Ferrari,Lloyd A. Greene +1 more
TL;DR: It is proposed that the neuroprotective activity of GM1 is due, at least in part, to its ability to favor the dimerization of neurotrophic factor receptor tyrosine kinases and thereby mimicking the action of their corresponding ligands.
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Neuroprotection by NGF in the PC12 In Vitro OGD Model
TL;DR: Findings support the notion that pretreatment with NGF confers neuroprotection from OGD insult, a phenomenon coincidentally related to differential inhibition of MAPK stress kinase isoforms and differential gene expression.
71
Nerve growth factor and forskolin prevent H2O2-induced apoptosis in PC12 cells by glutathione independent mechanism
TL;DR: Exogenous expression of an oncogenic ras suppressed apoptosis caused by H2O2 indicating that Ras protein also plays a role in suppressing apoptosis causing by oxidative radical stress.
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Nerve Growth Factor–specific Regulation of Protein Methylation during Neuronal Differentiation of PC12 Cells
TL;DR: The results indicate that NGF regulates the methylation of several specific proteins and that protein methylation is involved in neurite outgrowth from PC12 cells.
References
Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor.
TL;DR: A single cell clonal line which responds reversibly to nerve growth factor (NGF) has been established from a transplantable rat adrenal pheochromocytoma and should be a useful model system for neurobiological and neurochemical studies.
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Effect of protein synthesis inhibitors on growth factor activation of c-fos, c-myc, and actin gene transcription.
TL;DR: The results suggest that in PC12 cells c-fos transcription is activated by a protein-synthesis-independent mechanism, whereas c-myc stimulation requires new protein synthesis.
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Selective and nonselective stimulation of central cholinergic and dopaminergic development in vitro by nerve growth factor, basic fibroblast growth factor, epidermal growth factor, insulin and the insulin-like growth factors I and II
TL;DR: NGF and, very similarly, bFGF seem to influence septal cholinergic neurons directly and rather selectively, whereas the neurotrophic actions of insulin and the insulin-like growth factors appear to be more general.
553
Effects of insulin, insulin-like growth factor-II, and nerve growth factor on neurite formation and survival in cultured sympathetic and sensory neurons
TL;DR: The hypothesis that insulin and its homologs belong to a broad family of neuritogenic polypeptides is supported, as it is shown that insulin acts on the same, or a subpopulation, of NGF-responsive neurons.
453
Sarcoma viruses carrying ras oncogenes induce differentiation-associated properties in a neuronal cell line
Makoto Noda,Minoru S.H. Ko,Akihiko Ogura,Ding Gan Liu,Takehiko Amano,Toshiya Takano,Yoji Ikawa +6 more
TL;DR: It is found that Ki- and Ha-MSV mimic some, if not all, of the activities of NGF in PC12 cells, and there is evidence that the viral oncogenes, v-Ki-ras and v-Ha-ras, are responsible for this phenomenon.
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