EGF enhances the survival of dopamine neurons in rat embryonic mesencephalon primary cell culture

Casper, Diana; Mytilineou, Catherine; Blum, Mariann

doi:10.1002/jnr.490300213

Cited by 176 publications

(90 citation statements)

References 49 publications

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“…[54][55][56][57] Previous neurobiological studies have demonstrated that peptides from the EGF family exert neurotrophic effects on developing dopaminergic neurons in vitro and in vivo. 4,[13][14][15][16] In embryonic mesencephalon culture, EGF specifically enhances cell survival of dopamine neurons. 13 Intraventricular infusion of EGF elevates striatal innervation by dopaminergic fibers from the substantia nigra.…”

Section: Discussionmentioning

confidence: 99%

“…4,[13][14][15][16] In embryonic mesencephalon culture, EGF specifically enhances cell survival of dopamine neurons. 13 Intraventricular infusion of EGF elevates striatal innervation by dopaminergic fibers from the substantia nigra. 15 This is consistent with findings from TGF␣-null-mutant mice, which have decreased numbers of midbrain dopaminergic neurons.…”

Section: Discussionmentioning

confidence: 99%

“…[10][11][12] EGF and structurally related peptides have been studied extensively with respect to the growth and survival of midbrain dopaminergic neurons. 4,[13][14][15][16]18 Gene-targeting studies have confirmed the importance of EGF in the general development of brain structures as well as in monoaminergic function. [17][18][19][20] Observations in transgenic mice overexpressing TGF␣ emphasize the biologic significance of the EGF family for the development and function of monoaminergic neurons.…”

Section: Introductionmentioning

confidence: 99%

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Abnormal expression of epidermal growth factor and its receptor in the forebrain and serum of schizophrenic patients

et al. 2002

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Epidermal growth factor (EGF) comprises a structurally related family of proteins containing heparin-binding EGF-like growth factor (HB-EGF) and transforming growth factor alpha (TGF␣) that regulates the development of dopaminergic neurons as well as monoamine metabolism. We assessed the contribution of EGF to schizophrenia by measuring EGF family protein levels in postmortem brains and in fresh serum of schizophrenic patients and control subjects. EGF protein levels were decreased in the prefrontal cortex and striatum of schizophrenic patients, whereas the levels of HB-EGF and TGF␣ were not significantly different in any of the regions examined. Conversely, EGF receptor expression was elevated in the prefrontal cortex. Serum EGF levels were markedly reduced in schizophrenic patients, even in young, drug-free patients. Chronic treatment of animals with the antipsychotic drug haloperidol had no influence on EGF levels in the brain or serum. These findings suggest that there is abnormal EGF production in various central and peripheral tissues of patients with both acute and chronic schizophrenia. EGF might thus provide a molecular substrate for the pathologic manifestation of the illness, although additional studies are required to determine a potential link between impaired EGF signaling and the pathology/etiology of schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Abnormal expression of epidermal growth factor and its receptor in the forebrain and serum of schizophrenic patients

et al. 2002

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“…Cells were scraped off the culture wells and counted by liquid scintillation spectrometry. Serotonin uptake was estimated similarly (Casper et al, 1991), using 20 nM 5-[3H]-hydroxytryptamine instead of DA. Blank values were determined in the presence of 3 jiM citalopram (Lundbeck and Co., Copenhagen, Denmark).…”

Section: Neurotransmitter Uptakementioning

confidence: 99%

Rescue of Mesencephalic Dopamine Neurons by Anticancer Drug Cytosine Arabinoside

Michel

Ruberg

Agid

1997

Journal of Neurochemistry

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Nanomolar concentrations of cytosine arabinoside (ara-C), a structural analogue of 2 '-deoxycytidine (2'dC) used in the chemotherapy of cancer, proved to be highly effective in preventing the death of postmitotic dopaminergic neurons that occurs spontaneously by apoptosis in mesencephalic cultures. The rescued cells were totally functional and highly differentiated. The trophic/neuroprotective effects of ara-C were (1) specific for dopaminergic neurons; (2) long-lived, remaining detectable several days after withdrawal of the nucleoside analogue from the culture medium; (3) still observed when the treatment was delayed after plating; (4) abolished by an excess of 2'dC or dCTP, or by exposure to the neurotoxin 1-methyl-4-phenylpyridinium; and (5) mimicked by ara-CTP, 5-fluoro-2 '-deoxyuridine, and aphidicolin. Autoradiographic studies revealed that ara-C was incorporated exclusively into astrocyte nuclei, suggesting that the dopaminotrophic activity was indirect and resulted from the antiproliferative action of the modified nucleoside on glial cells at concentrations that were not neurotoxic. No evidence was found for putative deleterious or trophic molecules secreted by proliferating or ara-C-treated astrocytes, respectively, suggesting that neuroglial contact may play a role. Our results suggest a possible mechanism underlying neurodegeneration in Parkinson's disease, where selective loss of dopaminergic neurons in the mesencephalon is accompanied by astrogliosis.

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“…De hecho, se demostró que actúa como un factor neurotrófico sobre neuronas cultivadas de la corteza cerebral, del telencéfalo subneocortical y del cerebelo, incrementando el crecimiento neurona1 y la supervivencia (5-7). Su acción neurotrófica sobre las neuronas dopaminérgicas se describió como un incremento de la supervivencia y de la maduración (8,9).…”

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Acción del factor de crecimiento epidérmico sobre el desarrollo de las células estriatales cultivadas

et al. 1996

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ResumenEn este trabajo se describe la acción del factor de crecimiento epidérmico (FCE) sobre las células del estriado embrionario en un sistema de cultivo disociado de neuronas y glías. El cultivo de células se preparó a partir de embriones de ratas de 16-17 días. En el sistema de cultivo empleado, la población celular fue cultivada durante 20-24 horas en un medio que contenía suero y, posteriormente, fue tratada con 20 ng/mL del FCE en un medio libre de suero. La eliminación del suero en este período inicial de desarrollo provocó una disminución apreciable de las células vivas en los cultivos tratados y en los controles. Al parecer, la población de células sobrevivientes estaba integrada, en su mayoría, por precursores celulares teniendo en cuenta su capacidad proliferativa. La acción del FCE sobre las células se manifestó en un aumento del número de células debido fundamentalmente a un estímulo de la proliferación de los precursores neuronales y astrocitos. Este efecto estuvo acompañado por una reducción de la diferenciación morfológica neuronal cuando se comparó con los cultivos controles. En los cultivos, a los 16 días, la detección de la actividad específica de la colina acetiltrasferasa evidenció la diferenciación de una subpoblación neuronal colinérgica, las cuales respondieron al tratamiento con el factor de crecimiento nervioso con un aumento de la actividad de la enzima. SummaryThis paper describes the effect of epidermal growth factor (EGF) on embryonic striatal cells in mixed neuronal-glial cultures prepared from 16-17 day old rat embryos. In the culture system employed, cell population was cultured for 20-24 hours in serum supplemented medium prior to being treated with 20 ng/mL epidermal growth factor (EGF) serum-free medium. This early withdrawal of serum from the culture medium caused an appreciable decline of viable cells in both control and treated cultures. It seems that the majority of surviving cells were precursors, taking into account their proliferative capacity. EGF action on cell population provoked an increase in cell numbers, mainly due to the stimulation of neuronal precursor and and astrocyte proliferation. This increase in cell proliferation was accompanied by neuronal morphological differentiation delay when compared to control cultures. Choline acetyltransferase specific activity detected in 16-day old cultures, showed the differentiation of a cholinergic neuronal subpopulation, which responded to nerve growth factor treatment with enhanced enzyme activity.

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EGF enhances the survival of dopamine neurons in rat embryonic mesencephalon primary cell culture

Cited by 176 publications

References 49 publications

Abnormal expression of epidermal growth factor and its receptor in the forebrain and serum of schizophrenic patients

Abnormal expression of epidermal growth factor and its receptor in the forebrain and serum of schizophrenic patients

Rescue of Mesencephalic Dopamine Neurons by Anticancer Drug Cytosine Arabinoside

Acción del factor de crecimiento epidérmico sobre el desarrollo de las células estriatales cultivadas

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