Epidermal growth factor and the nervous system

Plata‐Salamán, Carlos R.

doi:10.1016/0196-9781(91)90115-6

Cited by 114 publications

(60 citation statements)

References 148 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…EGF induces the expression of TH to enhance DA synthesis in cultured midbrain neurons. 4,5 To confirm the neurochemical effects of exogenous EGF in the intact brain, EGF was administered subcutaneously every other day until postnatal day 10 and the same dose of cytochrome c was similarly injected into control littermates. Protein levels of TH as well as those of the neuronal and glial markers, NSE and GFAP, were determined by immunoblotting using neocortical and striatum specimens from EGF-treated rats on postnatal day 11.…”

Section: Resultsmentioning

confidence: 99%

“…2,3 In the central nervous system, EGF enhances survival and promotes the differentiation of neurons, particularly midbrain dopaminergic neurons. [4][5][6][7] In fact, the ubiquitous presence of EGF receptors (EGFRs) in both developing and mature brain neurons supports the biological significance of the activities of EGF and/or its related molecules in postmitotic neurons. 8,9 Studies utilizing gene-targeting or transgenic strategies to study the EGF gene family have confirmed their importance in prenatal and postnatal development of brain structures as well as in monoamine pharmacology.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development

et al. 2003

View full text Add to dashboard Cite

Epidermal growth factor (EGF) and its structurally related proteins are implicated in the developmental regulation of various brain neurons, including midbrain dopaminergic neurons. There are EGF and EGF receptor abnormalities in both brain tissues and blood from schizophrenic patients. We administered EGF to neonatal rats to transiently perturb endogenous EGF receptor signaling and evaluated the neurobehavioral consequences. EGF-treatment-induced transient impairment in tyrosine hydroxylase expression. The animals grew normally, exhibited normal weight increase, glial growth, and gross brain structures, and later lost the tyrosine hydroxylase abnormality. During and after development, however, the rats began to display various behavioral abnormalities. Abnormal sensorimotor gating was apparent, as measured by deficits in prepulse inhibition of acoustic startle. Motor activity and social interaction scores of the EGF-treated animals were also impaired in adult rats, though not in earlier developmental stages. In parallel, there was a significant abnormality in dopamine metabolism in the brain stem of the adult animals. Gross learning ability appeared to be normal as measured by active avoidance. These behavioral alterations, which are often present in schizophrenic models, were ameliorated by subchronic treatment with clozapine. Although the molecular and/or physiologic background(s) of these behavioral abnormalities await further investigation, the results of the present experiment indicate that abnormal EGF receptor stimulation given during limited neonatal stages can result in severe and persistent cognitive/behavioral dysfunctions, which appear only in adulthood.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development

et al. 2003

View full text Add to dashboard Cite

show abstract

“…3A and 4). Together, these findings indicate that PD173952 and PP1 do not directly inhibit ErbB1 RTK activity in NHKs in response to low ligand concentrations expected to be encountered in physiological conditions (Plata-Salaman, 1991). However, it remains possible that these compounds may be acting by interfering with the ability of Src family kinases or other unidentified kinases to promote tyrosine phosphorylation of ErbB1 after stimulation of NHKs with high concentrations of EGF.…”

Section: Sfks Regulate Autocrine Erbb Signaling In Keratinocytes 1153mentioning

confidence: 87%

Src Family Kinase Inhibitors Block Amphiregulin-Mediated Autocrine ErbB Signaling in Normal Human Keratinocytes

Kansra¹,

Stoll²,

Johnson³

et al. 2005

Molecular Pharmacology

View full text Add to dashboard Cite

c-Src potentiates proliferation, survival, and invasiveness in response to epidermal growth factor (EGF) in human mammary carcinoma cells. Tyrosine (Tyr) 845 of ErbB1 is phosphorylated by Src and has been implicated in control of malignant behavior. Although several lines of evidence also suggest important interactions of ErbB and Src family kinase signaling in normal epithelial cells, little is known about the mechanism of this interaction. Studying normal human keratinocytes (NHKs), here we demonstrate strong expression of the Src family kinases Src, Yes, and Fyn; Src family kinase-dependent stimulation of Tyr 845 by EGF; and potent inhibition of NHK proliferation and migration by two Src family kinase inhibitors PP1 and PD173952. EGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation occurred at much lower concentrations of EGF than required to phosphorylate Tyr 845. Moreover, the effect of Src family kinase inhibitors on EGFstimulated ERK phosphorylation was transient, prompting a search for other targets of Src family kinase action. By enzymelinked immunosorbent assay analysis, we found that three different Src family kinase inhibitors [6-(2,6-, and 2-oxo-3-(4,5,6,7-tetrahydro-1H-indol-2-ylmethylene)-2,3-dihydro-1H-indole-5-sulfonic acid dimethylamide (SU6656)] markedly inhibited elaboration of soluble amphiregulin by NHKs. The ErbB inhibitor PD158780 and the mitogen-activated protein kinase kinase inhibitor U0126 also markedly inhibited NHK proliferation, migration, and amphiregulin production. Together, these observations demonstrate that one or more Src family kinases act upstream as well as downstream of ErbB1 to promote amphiregulin-dependent autocrine stimulation of NHKs and suggest that autocrine NHK proliferation is more dependent upon ERK activation than upon Tyr 845 phosphorylation.

show abstract

“…In this study, the number of newborn cells that labelled by mature-neuron marker NeuN was higher at P10-16, corresponding to the early stage of the brain development. Some researches has demonstrated that many growth factors are expressed at high levels in the developing brain and decreased when the brain development completed [19,20] . Moreover, our study also found that in the early development stage, the cytogenesis varied in different areas of the brain.…”

Section: Discussionmentioning

confidence: 99%

Changes of cell proliferation and differentiation in the developing brain of mouse

et al. 2007

View full text Add to dashboard Cite

Objective To investigate the cell proliferation and differentiation in the developing brain of mouse. Methods C57/BL6 mice were divided into 3 groups at random. Bromodeoxyuridine (BrdU) was injected into the brains in different development periods once a day for 7 d. The brains were retrieved 4 weeks after the last BrdU injection. Immunohistochemical and immunofluorescent studies were carried out for detecting cell proliferation (BrdU) and cell differentiation (NeuN, APC, Iba1, and S100β), respectively. Results The number of BrdU labeled cells decreased significantly with the development of the brain. Cell proliferation was prominent in the cortex and striatum. A small portion of BrdU and NeuN double labeled cells could be detected in the cortex at the early stage of development, and in the striatum and CA of the hippocampus in all groups. The majority of BrdU labeled cells were neuroglia, and the number of neuroglia cells decreased dramatically with brain maturation. Neurogenesis is the major cytogenesis in the dentate gyrus. Conclusion These results demonstrated that cell proliferation, differentiation and survival were age and brain region related.

show abstract

Epidermal growth factor and the nervous system

Cited by 114 publications

References 148 publications

Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development

Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development

Src Family Kinase Inhibitors Block Amphiregulin-Mediated Autocrine ErbB Signaling in Normal Human Keratinocytes

Changes of cell proliferation and differentiation in the developing brain of mouse

Contact Info

Product

Resources

About