Identification of Candidate Genes Induced by Retinoic Acid in Embryonal Carcinoma Cells

Cheung, William M.W.; Chu, Apple H.; Ip, Nancy Y.

doi:10.1046/j.1471-4159.1997.68051882.x

Cited by 21 publications

(11 citation statements)

References 32 publications

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“…Neuronal differentiation Cañon et al, 2004;Scheibe et al, 1991;Scheibe and Wagner, 1992 NT2 Edsjo et al, 2003;Encinas et al, 1999Encinas et al, , 2000Kaplan et al, 1993;Rossino et al, 1991;Wuarin et al, 1994 MN9D Bain et al, 1995;Gottlieb and Huettner, 1999;O'Shea, 2001;Bibel et al, 2004;Guan et al, 2001 Novitch et al, 2003;Sockanathan et al, 2003;Sockanathan and Jessell, 1998 Edsjo et al, 2003;Kaplan et al, 1993;Lucarelli et al, 1995;Malek and Halvorsen, 1997;Merrill et al, 2002Merrill et al, , 2005Rossino et al, 1991 P19 cell line Stra1, Stra3 and more Bouillet et al, 1995;Oulad-Abdelghani et al, 1997 RARs, RXRs, nuclear matrix associated protein; synergistic effects with neurotrophins and more Cheung et al, 2000aCheung et al, ,b, 2005Cheung and Ip, 2000;Wuarin et al, 1994 PC3 human prostate carcinoma cell line IGFBP-3, -5 (up) Hwa et al, 1997 F9 embryonal carcinoma cell line FGF-3 (up) Murakami et al, 1999 Myeloma cells, osteoblasts IL-6, IL-6R (down) Chen et al, 1999;Smith et al, 1998;refs. expression of IL-6 is suppressed or enhanced depending on the cell culture system. While the production of IL-1 itself may be supported by retinoids, RA counteracts downstream effects, for instance the IL-1-induced synthesis of other cytokines (Gross et al, 1993).…”

Section: Expression Of Cytokinesmentioning

confidence: 99%

New therapeutic target for CNS injury? The role of retinoic acid signaling after nerve lesions

Mey

2006

J. Neurobiol.

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Experiments with sciatic nerve lesions and spinal cord contusion injury demonstrate that the retinoic acid (RA) signaling cascade is activated by these traumatic events. In both cases the RA-synthesizing enzyme is RALDH-2. In the PNS, lesions cause RA-induced gene transcription, intracellular translocation of retinoid receptors, and increased transcription of CRBP-I, CRABP-II, and retinoid receptors. The activation of RARbeta appears to be responsible for neurotrophic and neuritogenic effects of RA on dorsal root ganglia and embryonic spinal cord. While the physiological role of RA in the injured nervous system is still under investigation three domains of functions are suggested: (1) neuroprotection and support of axonal growth, (2) modulation of the inflammatory reaction by microglia/macrophages, and (3) regulation of glial differentiation. Few studies have been performed to support nerve regeneration with RA signals in vivo, but a large number of experiments with neuronal and glial cell cultures and spinal cord explants point to beneficial effects of RA, so that future therapeutic approaches will likely focus on the activation of RA signaling.

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Section: Expression Of Cytokinesmentioning

confidence: 99%

New therapeutic target for CNS injury? The role of retinoic acid signaling after nerve lesions

Mey

2006

J. Neurobiol.

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“…At the nucleic acid level differential gene expression has been reported already [1][2][3][4][5][6][7][8][9]. However important studies at the RNA level may be, no conclusions about the quantity of protein expression and protein levels can be drawn in the majority of observations and the presence of post-translational modifications cannot be determined by gene techniques.…”

Section: Introductionmentioning

confidence: 99%

Proteins involved in neuronal differentiation of neuroblastoma cell line N1E‐115

Freilinger

Gelpí

et al. 2007

Electrophoresis

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Neuronal differentiation (ND) represents a well-defined phenomenon in biological terms but proteins involved have not been studied systematically. We therefore aimed to study ND by retinoic acid (RA) in a widely used neuroblastoma cell line by comparative proteomics. The ND was induced in the N1E-115 cell line by serum deprivation and RA treatment. Undifferentiated cells and cells undergoing serum deprivation served as controls. Protein extracts were run on 2-DE followed by MALDI-TOF or MALDI-TOF-TOF analysis. Quantification was carried out using specific software and stringent statistical analysis was performed. Tubulin beta 5, cat eye syndrome critical region protein 5 homolog, putative GTP-binding protein PTD004 homolog, and the metabolic proteins glyceraldehyde-3-phosphate dehydrogenase and transketolase were differentially regulated. Differential protein levels of cytoskeleton proteins including tubulins and metabolic proteins have been reported to be regulated by ND. Herein, specific signaling differences as reflected by putative GTP-binding protein PTD004 changes in differentiated cells are shown and a possible role for the Cat eye syndrome critical region protein 5 homolog is proposed. The protein disulfide isomerase associated 3 protein fits the already proposed findings of chaperon regulation by ND. The study forms the molecular basis for further evaluation of the functional roles of the differentially expressed proteins in ND.

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“…NT2 cells, a human embryonal carcinoma cell line, become post-mitotic CNS neurons upon treatment with retinoic acid (RA; Andrews 1984). Accumulating evidence supports the use of NT2 cells as an in vitro model to study the process of early neuronal differentiation in the CNS (Miller et al 1990;Abraham et al 1991;Moasser et al 1995;Cheung et al 1997Cheung et al , 2000Cheung et al , 2001. While the conventional methodology normally requires at least 2 months to obtain mature neurons, we have recently developed a rapid protocol to differentiate NT2 cells using cell aggregation and RA (Cheung et al 1999).…”

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confidence: 99%

Expression of Cdk5 and its activators in NT2 cells during neuronal differentiation

Wang

2002

Journal of Neurochemistry

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We have recently developed a rapid protocol involving NT2 cell aggregation and treatment with retinoic acid (RA) to produce terminally differentiated CNS neurons. As a first step to explore the functional roles of cell-cycle regulatory proteins in the process of neuronal differentiation, the expression profiles of cyclin-dependent kinases (Cdks) and their regulators were examined in NT2 cells following treatment with RA. One of the Cdks, Cdk5, has been demonstrated to affect the process of neuronal differentiation and suggested to play an important role in development of the nervous system. We found that the expression of Cdk5 was gradually increased, while its activators (p35 and p39) as well as Cdk5 kinase activity were induced in NT2 cells during the process of neuronal differentiation. Moreover, both p35 and p39 were localized along the axons and varicosity-like structures of differentiated NT2 neurons. Taken together, our results demonstrated that NT2 cells provide a good in vitro model system to examine signaling pathways involved in the regulation of Cdk5 activators and to elucidate the functional roles of Cdk5 in neuronal differentiation.

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Identification of Candidate Genes Induced by Retinoic Acid in Embryonal Carcinoma Cells

Abstract: Retinoic acid (RA) induced the terminal differentiation of a human embryonal carcinoma cell line (NT2/ Dl) into several morphologically distinct cell types, including the postmitotic CNS neurons.

Cited by 21 publications

References 32 publications

New therapeutic target for CNS injury? The role of retinoic acid signaling after nerve lesions

New therapeutic target for CNS injury? The role of retinoic acid signaling after nerve lesions

Proteins involved in neuronal differentiation of neuroblastoma cell line N1E‐115

Expression of Cdk5 and its activators in NT2 cells during neuronal differentiation

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