The epidermal growth factor.

Boonstra, Johannes; Rijken, P.J.; Humbel, Bruno M.; Cremers, Fons; Verkleij, Arie J.; Henegouwen, Paul van Bergen en

doi:10.1006/cbir.1995.1086

Cited by 269 publications

(94 citation statements)

References 68 publications

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“…It is well known that tyrosine kinase receptors and specifically EGFR can be activated both by cell swelling or shrinkage [43,44] and can modulate numerous intracellular signaling pathways, such as focal adhesion kinase, mitogenactivated protein (MAP) kinase (MAPK), or phosphoinositide-3 kinase (PI3K) [45,46]. Our data indicate that EGFR signaling downstream of GABA A Rs promotes cell cycle entry of prominin þ precursors rather than a change in their cycle kinetics.…”

Section: Discussionmentioning

confidence: 69%

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

et al. 2011

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Signal-regulated changes in cell size affect cell division and survival and therefore are central to tissue morphogenesis and homeostasis. In this respect, GABA receptors (GABA A Rs) are of particular interest because allowing anions flow across the cell membrane modulates the osmolyte flux and the cell volume. Therefore, we have here investigated the hypothesis that GABA may regulate neural stem cell proliferation by inducing cell size changes. We found that, besides neuroblasts, also neural precursors in the neonatal murine subependymal zone sense GABA via GABA A Rs. However, unlike in neuroblasts, where it induced depolarization-mediated [Ca 21 ] i increase, GABA A Rs activation in precursors caused hyperpolarization. This resulted in osmotic swelling and increased surface expression of epidermal growth factor receptors (EGFRs). Furthermore, activation of GABA A Rs signaling in vitro in the presence of EGF modified the expression of the cell cycle regulators, phosphatase and tensin homolog and cyclin D1, increasing the pool of cycling precursors without modifying cell cycle length. A similar effect was observed on treatment with diazepam. We also demonstrate that GABA and diazepam responsive precursors represent prominin 1 stem cells. Finally, we show that as in in vitro also in in vivo a short administration of diazepam promotes EGFR expression in prominin 1 stem cells causing activation and cell cycle entry. Thus, our data indicate that endogenous GABA is a part of a regulatory mechanism of size and cell cycle entry of neonatal stem cells. Our results also have potential implications for the therapeutic practices that involve exposure to GABA A Rs modulators during neurodevelopment. STEM CELLS 2011;29:307-319 Disclosure of potential conflicts of interest is found at the end of this article.

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Section: Discussionmentioning

confidence: 69%

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

et al. 2011

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“…These data demonstrated that the EGF receptor tyrosine kinase serves as an important effector in a signaling pathway connecting mGluR5 to JNK. EGF receptors undergo a rapid, intramolecular dimerization and autophosphorylation at specific C-terminal tyrosine residues, including tyrosine 1173, after ligand activation (Downward et al, 1984;Boonstra et al, 1995). Activation of G-proteincoupled receptors also transactivates the EGF receptor by increasing its tyrosine autophosphorylation (Peavy et al, 2001).…”

Section: Transactivation Of Egf Receptors Is Required For Mglur5-medimentioning

confidence: 99%

A Signaling Mechanism from Gαq-Protein-Coupled Metabotropic Glutamate Receptors to Gene Expression: Role of the c-Jun N-Terminal Kinase Pathway

Yang¹,

Mao²,

Chen³

et al. 2006

J. Neurosci.

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G␣q-protein-coupled group I metabotropic glutamate receptors (mGluRs) are densely expressed in brain neurons and are actively involved in various cellular activities. In this study, we investigated the role of group I mGluRs in regulating the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase in cultured neurons. We found that selective activation of mGluR5 induced a rapid and transient phosphorylation of JNK. In a series of studies to determine the mechanisms, we found that the conventional mGluR5-associated signaling pathways (inositol-1,4,5-triphosphate-mediated Ca 2ϩ release and activation of protein kinase C) were not involved in the mGluR5 regulation. Instead, ligand stimulation of mGluR5 caused a dynamic transactivation of the epidermal growth factor (EGF) receptor, which in turn triggered a downstream signaling pathway to upregulate JNK phosphorylation. Furthermore, the mGluR5-dependent JNK activation specifically activated c-Jun, but not activating transcription factor-2 or JunD, and increased activator protein-1 (AP-1)-mediated endogenous transcriptional activity. Together, we identified a novel mGluR5-to-nucleus communication through the EGF/JNK pathway, which functions to regulate AP-1-mediated transcription.

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“…(In our unpublished data we have also included other cytokines, such as IL-4, IL-8, and 1155 IL-10, for the studies, and all of them showed no specific change). The fact that the expression of EGFR mRNA increased in the 2 to 3 weeks after EBV infection and then gradually decreased to the original level by 4 weeks after infection indicates that EBV infection activates the host cellular EGFR expression, which may result in an increase in the rate of cellular proliferation through a paracrine or autocrine pathway (Boonstra et al, 1995;Santini et al, 1991;Zheng et al, 1994).…”

Section: Identification Of Mrna Expression Of Growth Factors/cytokinementioning

confidence: 99%

Response of Nasopharyngeal Carcinoma Cells to Epstein-Barr Virus Infection In Vitro

Lin

Kao

Lin

et al. 2000

Laboratory Investigation

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SUMMARY:Many nasopharyngeal carcinoma (NPC) biopsy specimens contain Epstein-Barr virus (EBV). However, the response of NPC cells to EBV infection in vitro and in vivo is not well characterized. In this experiment we infected NPC cells with EBV particles through endocytosis of a complex of EBV immunoglobulin A (IgA) secretory component (SC) protein to observe the response of host cells to the foreign viral infection in vitro. We found that EBV particles were endocytosed and stabilized in NPC nuclei 24 hours after infection; the EBV genomes were then gradually decreased after serial passages within 3 to 4 weeks by the following pathway: the EBV genomes first moved toward the nuclear envelope from the center of the nucleus; after crossing the nuclear envelope, they moved into the cytoplasm and toward the plasma membrane and were discharged by exocytosis. At the 10th day of EBV infection, EBV-latent membrane protein-1 and Epstein-Barr nuclear antigen (EBNA)-1 protein expressions could be detected, but not EBV-viral capsid antigen. Observation of EBNA-1 protein and host growth factor and cytokine gene expressions in the weeks after incubation revealed that the EBNA-1 protein expression was decreased proportionally with decrease of EBV genome. The mRNA expression of epithelial growth factor receptor, transforming growth factor (TGF)-␣, interleukin (IL)-1␤, IL-6, and granulocyte-macrophage colony-stimulating factor increased within 1 to 2 weeks after infection, and gradually recovered to the original level at 3 to 4 weeks, whereas the mRNAs of TGF␤1, TGF␤ receptor type I (TGF␤RI), TGF␤R type II, IL-8, and tumor necrosis factor-␣ remained unchanged. It is concluded that in vitro EBV infection in NPC cells results in increase of certain growth factor and cytokine gene expressions in host cells. The change in gene expression returns to the original level approximately 3 to 4 weeks after infection because of exocytosis of EBV DNA by the infected cells through an unidentified mechanism. (Lab Invest 2000, 80:1149-1160.N asopharyngeal carcinoma (NPC) is one of the most common cancers among Chinese living in Taiwan, Singapore, and South China (Chan, 1990;de The, 1982; Lin et al, 1971). The etiological factors for this cancer are not yet well defined. Epstein-Barr virus (EBV) has been suggested to be closely associated with NPC (Ablashi et al, 1991;Klein et al, 1974;Niedobitek et al, 1991;Zur Hausen et al, 1970). Hereditary and other environmental factors, such as eating salted fish and exposure to sulfuric acid vapor, have also been associated with NPC (Armstrong et al, 1983;Hirayama and Ito, 1981;Ho et al, 1999).For identification of the actual relationship between EBV and NPC, we have previously established nine NPC cell lines in our laboratory (Lin et al, 1990(Lin et al, , 1993.Results from the observation of EBV in these nine NPC cell lines and biopsy specimens revealed that EBV was present in only five of nine lines and was an episomal, but not an integrated form, in the infected cells. In each EBV-infected cell line, on...

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The epidermal growth factor.

Cited by 269 publications

References 68 publications

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

A Signaling Mechanism from Gαq-Protein-Coupled Metabotropic Glutamate Receptors to Gene Expression: Role of the c-Jun N-Terminal Kinase Pathway

Response of Nasopharyngeal Carcinoma Cells to Epstein-Barr Virus Infection In Vitro

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