Ultrastructural and transcriptional profiling of neuropathological misregulation of CREB function

Valor, L M; Jancic, D; Lujan, R; Barco, A

doi:10.1038/cdd.2010.40

Cited by 28Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchNeurological Disease Mechanisms and Treatments

Ultrastructural and transcriptional profiling of neuropathological misregulation of CREB function

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Valor, L M, Jancic, D, Lujan, R, Barco, A·2010·Cell Death & Differentiation

DOI 10.1038/cdd.2010.40

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Abstract

We compare here the neurodegenerative processes observed in the hippocampus of bitransgenic mice with chronically altered levels of cAMP-response element-binding protein (CREB) function. The combination of genome-wide transcriptional profiling of degenerating hippocampal tissue with microscopy analyses reveals that the sustained inhibition of CREB function in A-CREB mice is associated with dark neuron degeneration, whereas its strong chronic activation in VP16-CREB mice primarily causes excitotoxic cell death and inflammation. Furthermore, the meta-analysis with gene expression profiles available in public databases identifies relevant common markers to other neurodegenerative processes and highlights the importance of the immune response in neurodegeneration. Overall, these analyses define the ultrastructural and transcriptional signatures associated with these two forms of hippocampal neurodegeneration, confirm the importance of fine-tuned regulation of CREB-dependent gene expression for CA1 neuron survival and function, and provide novel insight into the function of CREB in the etiology of neurodegenerative processes.

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Removing the creb1 gene in adult mouse forebrain or chronic inhibition of CREB function leads to extensive neurodegeneration in the hippocampus.
“Removing the creb1 gene in adult mouse forebrain or chronic inhibition of CREB function leads to extensive neurodegeneration in the hippocampus (67,68).”
From CREB-activity and nmnat2 transcription are down-regulated prior to neurodegeneration, while NMNAT2 over-expression is neuroprotective, in a mouse model of human tauopathy (2012) · cites this paper as [68]
The section “Chronic inhibition of CREB function causes dark neuron degeneration” reports CA1 neuron loss in mice expressing the CREB inhibitor A-CREB, supporting the chronic-inhibition part of the sentence. The passages do not report removal of the creb1 gene in adult mouse forebrain, so this source does not support that part. (LLM, conf=0.88)
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Authors: Valor, L. M., Jancic, D., Lujan, R., & Barco, A.
Affiliations: Consejo Superior de Investigaciones Científicas (ES)
Corresponding author: Valor, L M
ORCID: Valor, L M
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2010-04-16
Volume: 17
Issue: 10
Pages: 1636-1644
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/cdd.2010.40
OpenAlex: W1966615413
Cited by: 28
References: 40
Citations by year: 2023: 1 · 2022: 3 · 2021: 1 · 2019: 1 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 1 · 2012: 4
FWCI: 1.92
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Cell Death and Differentiation (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion, other-oa)
DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
Funders: European Commission
Generalitat Valenciana
Ministerio de Ciencia e Innovación (CSD2007-00023, SAF2008-00611)
Junta de Comunidades de Castilla-La Mancha
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: CREB, hippocampal neurodegeneration, CA1 neurons, excitotoxic cell death, neuroinflammation, gene expression profiling, gene expression signatures, neuronal ultrastructure
MeSH terms: Animals, Hippocampus, Inflammation, Mice, Transgenic, Nerve Degeneration, Neurons, Recombinant Fusion Proteins, Apoptosis, Cyclic AMP Response Element-Binding Protein, Herpes Simplex Virus Protein Vmw65, Gene Expression Profiling, Mice

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Ultrastructural and transcriptional profiling of neuropathological misregulation of CREB function

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