Early Phase of Plasticity-Related Gene Regulation and SRF Dependent Transcription in the Hippocampus

Iacono, Giovanni; Altafini, Claudio; Torre, Vincent

doi:10.1371/journal.pone.0068078

Cited by 10 publications

(8 citation statements)

References 196 publications

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“…The SRF-mediated regulation of these transcription factors seems to be rather common and conserved regardless of different cell types. Indeed, the involvement of SRF inferred by CIDER in the regulation of this cluster is consistent with the results of a similar study on hippocampal rat cells 16 , where a time-series cluster analysis of a set of 33 genes identified a subset of genes, including FOS , EGR1 , EGR2 , EGR4 , DUSP1 and NR4A1 , enriched for the SRF binding motif. Chromatin Immunoprecipitation (ChIP) experiments confirmed that SRF was binding to the promoters of FOS , EGR1 , EGR2 and NR4A1 16 .…”

Section: Resultssupporting

confidence: 90%

Promoter-level expression clustering identifies time development of transcriptional regulatory cascades initiated by ErbB receptors in breast cancer cells

Mina

Magi

Jurman

et al. 2015

Sci Rep

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The analysis of CAGE (Cap Analysis of Gene Expression) time-course has been proposed by the FANTOM5 Consortium to extend the understanding of the sequence of events facilitating cell state transition at the level of promoter regulation. To identify the most prominent transcriptional regulations induced by growth factors in human breast cancer, we apply here the Complexity Invariant Dynamic Time Warping motif EnRichment (CIDER) analysis approach to the CAGE time-course datasets of MCF-7 cells stimulated by epidermal growth factor (EGF) or heregulin (HRG). We identify a multi-level cascade of regulations rooted by the Serum Response Factor (SRF) transcription factor, connecting the MAPK-mediated transduction of the HRG stimulus to the negative regulation of the MAPK pathway by the members of the DUSP family phosphatases. The finding confirms the known primary role of FOS and FOSL1, members of AP-1 family, in shaping gene expression in response to HRG induction. Moreover, we identify a new potential regulation of DUSP5 and RARA (known to antagonize the transcriptional regulation induced by the estrogen receptors) by the activity of the AP-1 complex, specific to HRG response. The results indicate that a divergence in AP-1 regulation determines cellular changes of breast cancer cells stimulated by ErbB receptors.

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Section: Resultssupporting

confidence: 90%

Promoter-level expression clustering identifies time development of transcriptional regulatory cascades initiated by ErbB receptors in breast cancer cells

Mina

Magi

Jurman

et al. 2015

Sci Rep

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“…The effects of bicuculline suggest a role for enhanced excitatory transmission in the regulation of CCN1 mRNA levels. Similar results were obtained in organotypic hippocampal slices (Iacono et al, 2013 ). In vivo , CCN1 mRNA level increases with decreases in excitatory transmission that are caused by N -methyl-D-aspartate receptor inhibition (Ito et al, 2007 ).…”

Section: Expression and Functions Of Ccn Family Members In The Nervousupporting

confidence: 86%

Matricellular proteins of the Cyr61/CTGF/NOV (CCN) family and the nervous system

Malik

Liszewska

Jaworski

2015

Front. Cell. Neurosci.

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Matricellular proteins are secreted proteins that exist at the border of cells and the extracellular matrix (ECM). However, instead of playing a role in structural integrity of the ECM, these proteins, that act as modulators of various surface receptors, have a regulatory function and instruct a multitude of cellular responses. Among matricellular proteins are members of the Cyr61/CTGF/NOV (CCN) protein family. These proteins exert their activity by binding directly to integrins and heparan sulfate proteoglycans and activating multiple intracellular signaling pathways. CCN proteins also influence the activity of growth factors and cytokines and integrate their activity with integrin signaling. At the cellular level, CCN proteins regulate gene expression and cell survival, proliferation, differentiation, senescence, adhesion, and migration. To date, CCN proteins have been extensively studied in the context of osteo- and chondrogenesis, angiogenesis, and carcinogenesis, but the expression of these proteins is also observed in a variety of tissues. The role of CCN proteins in the nervous system has not been systematically studied or described. Thus, the major aim of this review is to introduce the CCN protein family to the neuroscience community. We first discuss the structure, interactions, and cellular functions of CCN proteins and then provide a detailed review of the available data on the neuronal expression and contribution of CCN proteins to nervous system development, function, and pathology.

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“…To confirm the microarray data, reverse transcriptase polymerase chain reaction (RT-PCR), an accepted method for validating microarray results in the neuroscience field [ 56 – 59 ], was applied to randomly up- and down-regulated genes using 3`-UTR specific gene primers ( S3 Table ). Briefly, total RNA samples were first DNase-treated with RNase-free DNase (QIAGEN, Maryland).…”

Section: Methodsmentioning

confidence: 99%

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus

et al. 2015

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Our six-week treadmill running training (forced exercise) model has revealed that mild exercise (ME) with an intensity below the lactate threshold (LT) is sufficient to enhance spatial memory, while intense exercise (IE) above the LT negates such benefits. To help understand the unrevealed neuronal and signaling/molecular mechanisms of the intensity-dependent cognitive change, in this rat model, we here investigated plasma corticosterone concentration as a marker of stress, adult hippocampal neurogenesis (AHN) as a potential contributor to this ME-induced spatial memory, and comprehensively delineated the hippocampal transcriptomic profile using a whole-genome DNA microarray analysis approach through comparison with IE. Results showed that only IE had the higher corticosterone concentration than control, and that the less intense exercise (ME) is better suited to improve AHN, especially in regards to the survival and maturation of newborn neurons. DNA microarray analysis using a 4 × 44 K Agilent chip revealed that ME regulated more genes than did IE (ME: 604 genes, IE: 415 genes), and only 41 genes were modified with both exercise intensities. The identified molecular components did not comprise well-known factors related to exercise-induced AHN, such as brain-derived neurotrophic factor. Rather, network analysis of the data using Ingenuity Pathway Analysis algorithms revealed that the ME-influenced genes were principally related to lipid metabolism, protein synthesis and inflammatory response, which are recognized as associated with AHN. In contrast, IE-influenced genes linked to excessive inflammatory immune response, which is a negative regulator of hippocampal neuroadaptation, were identified. Collectively, these results in a treadmill running model demonstrate that long-term ME, but not of IE, with minimizing running stress, has beneficial effects on increasing AHN, and provides an ME-specific gene inventory containing some potential regulators of this positive regulation. This evidence might serve in further elucidating the mechanism behind ME-induced cognitive gain.

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Early Phase of Plasticity-Related Gene Regulation and SRF Dependent Transcription in the Hippocampus

Cited by 10 publications

References 196 publications

Promoter-level expression clustering identifies time development of transcriptional regulatory cascades initiated by ErbB receptors in breast cancer cells

Promoter-level expression clustering identifies time development of transcriptional regulatory cascades initiated by ErbB receptors in breast cancer cells

Matricellular proteins of the Cyr61/CTGF/NOV (CCN) family and the nervous system

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus

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