Microarray analysis of the genes induced by tetracycline-regulated expression of NDRF/NeuroD2 in P19 cells

Oda, Hisanobu; Fushimi, Fumiyoshi; Kato, Masaki; Kitagawa, Masae; Araki, Kimi; Seki, Naohiko; Ohkubo, Hiroaki

doi:10.1016/j.bbrc.2005.07.093

Cited by 8 publications

(7 citation statements)

References 46 publications

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“…NeuroD2, a bHLH protein, plays important roles in neuronal development. In the presence of the NeuroD2 protein, Id1 was rapidly and significantly upregulated [ 51 ].…”

Section: Id Proteins With Various Pathophysiological Functionsmentioning

confidence: 99%

Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer’s Disease: Cell Cycle Reentry and Beyond

Chen

Yang

Lin

et al. 2020

Cells

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Inhibitor of DNA-binding/differentiation (Id) proteins, a family of helix-loop-helix (HLH) proteins that includes four members of Id1 to Id4 in mammalian cells, are critical for regulating cell growth, differentiation, senescence, cell cycle progression, and increasing angiogenesis and vasculogenesis, as well as accelerating the ability of cell migration. Alzheimer’s disease (AD), the most common neurodegenerative disease in the adult population, manifests the signs of cognitive decline, behavioral changes, and functional impairment. The underlying mechanisms for AD are not well-clarified yet, but the aggregation of amyloid-beta peptides (Aβs), the major components in the senile plaques observed in AD brains, contributes significantly to the disease progression. Emerging evidence reveals that aberrant cell cycle reentry may play a central role in Aβ-induced neuronal demise. Recently, we have shown that several signaling mediators, including Id1, hypoxia-inducible factor-1 (HIF-1), cyclin-dependent kinases-5 (CDK5), and sonic hedgehog (Shh), may contribute to Aβ-induced cell cycle reentry in postmitotic neurons; furthermore, Id1 and CDK5/p25 mutually antagonize the expression/activity of each other. Therefore, Id proteins may potentially have clinical applications in AD. In this review article, we introduce the underlying mechanisms for cell cycle dysregulation in AD and present some examples, including our own studies, to show different aspects of Id1 in terms of cell cycle reentry and other signaling that may be crucial to alter the neuronal fates in this devastating neurodegenerative disease. A thorough understanding of the underlying mechanisms may provide a rationale to make an earlier intervention before the occurrence of cell cycle reentry and subsequent apoptosis in the fully differentiated neurons during the progression of AD or other neurodegenerative diseases.

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“…NeuroD2, a bHLH protein, plays important roles in neuronal development. In the presence of the NeuroD2 protein, Id1 was rapidly and significantly upregulated [ 51 ].…”

Section: Id Proteins With Various Pathophysiological Functionsmentioning

confidence: 99%

Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer’s Disease: Cell Cycle Reentry and Beyond

Chen

Yang

Lin

et al. 2020

Cells

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“…Microarray analysis was recently performed to help elucidate the molecular mechanisms involved in toxicity [11][12][13] Here we analyzed gene expression profiles of TM4 mouse Sertoli cells after 1,3-DNB treatment and then analyzed canonical pathways of differentially expressed genes. Additionally, TM4 cells were treated with 2,5-hexanedione (2,5-HD), another reproductive toxicant targeting Sertoli cells, and transcriptional levels of genes selected from 1,3-DNB-treated samples were validated in both chemically treated TM4 cells by quantitative real-time polymerase chain reaction (PCR).…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiles of TM4 mouse Sertoli cells after 1,3-dinitrobenzene exposure and analysis of genes related to tight junction signaling pathways

Choi

Park

et al. 2010

BioChip J

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1,3-Dinitrobenzene (1,3-DNB) specifically injures Sertoli cells and induces testicular toxicity by disrupting the key function of these cells. To clarify the molecular mechanism underlying 1,3-DNB's action on Sertoli cells, we analyzed gene expression profiles of TM4 mouse Sertoli cells after chemical treatment. In total, 1,203 genes were identified as either up-or down-regulated, with greater than 1.5-fold changes (P⁄0.05). Based on k-means clustering, genes that were differentially expressed in a time-dependent manner were identified; then biofunction and canonical pathways were analyzed using Ingenuity Pathways Analysis. Genes related to axonal guidance, Nrf2-mediated oxidative stress response, protein ubiquitination, and tight junction signaling pathways were identified in either time-specifically or time-dependently regulated groups. The transcription levels of genes related to tight junction signaling pathways (Mpp5, F11r, Prkcz, Magi2, and Tgfb2) and genes encoding junction proteins (Ocln, Tjp1, Tjp2, Gja1, and Gjd2) were validated in 1,3-DNB-treated and 2,5-hexanedione-treated TM4 cells by quantitative real-time polymerase chain reaction. Comprehensive gene expression profiling of 1,3-DNB-treated TM4 cells and subsequent canonical pathway analyses provided valuable information regarding the molecular mechanism of cell death and cell interaction in TM4 mouse Sertoli cells after 1,3-DNB exposure.

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“…Thus far, few studies regarding toxicogenomic approaches for in vivo DES toxicity, particularly neonatal, have been performed. Microarray analyses have been applied extensively to elucidate the molecular mechanisms underlying organ-or tissue-specific toxicity [13][14][15][16] and carcinogenicity 17,18 . No reports, however, have been made on the genotoxic effects of DES using microarray technology.…”

Section: Introductionmentioning

confidence: 99%

Genotoxic effects of diethylstilbestrol on mouse Sertoli TM4 cells using gene expression profiling

Kim

et al. 2010

BioChip J

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Diethylstilbestrol (DES), a synthetic estrogen, was examined for genotoxicity in mouse testicular Sertoli TM4 cells using an in vitro micronucleus assay and microarray analysis to clarify the molecular mechanisms underlying the genotoxicity of estrogenic compounds on the male reproductive system. The micronucleus test showed that DES induced genotoxic effects on TM4 cells with S9 activation. Gene expression profiles were studied in DES-treated cells and positive controls, which were cyclophosphamide (CPA)-treated TM4 cells, as compared to the negative controls. In total, 349 and 328 genes were identified as being either up-or down-regulated, with over 2-fold changes, in DES-and CPA-treated TM4 cells, respectively. Biofunction and canonical pathways of differentially expressed genes were analyzed using Ingenuity Pathways Analysis, which were mainly categorized as cellular development and growth/proliferation. In addition, genes related to cell cycle regulation, such as Egr1, and Hdac11, were differentially expressed in DEStreated TM4 cells. A gene network analysis was also performed. Comprehensive gene expression profiling of DES-treated TM4 cells provides valuable information to better understand the genotoxic events of estrogenic chemicals in testicular Sertoli cells.

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Microarray analysis of the genes induced by tetracycline-regulated expression of NDRF/NeuroD2 in P19 cells

Cited by 8 publications

References 46 publications

Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer’s Disease: Cell Cycle Reentry and Beyond

Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer’s Disease: Cell Cycle Reentry and Beyond

Gene expression profiles of TM4 mouse Sertoli cells after 1,3-dinitrobenzene exposure and analysis of genes related to tight junction signaling pathways

Genotoxic effects of diethylstilbestrol on mouse Sertoli TM4 cells using gene expression profiling

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