Evidence map›Paper›PMID 29187362›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018

IKK2/NF-κB signaling protects neurons after traumatic brain injury.

Melanie Mettang, Stephanie Nadine Reichel, Michael Lattke, Annette Palmer, Alireza Abaei, Volker Rasche, Markus Huber-Lang, Bernd Baumann, Thomas Wirth

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 79 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Melanie MettangInstitute of Physiological Chemistry, Ulm University, Ulm, Germany.
Stephanie Nadine ReichelInstitute of Physiological Chemistry, Ulm University, Ulm, Germany.
Michael LattkeInstitute of Physiological Chemistry, Ulm University, Ulm, Germany.
Annette PalmerInstitute of Clinical and Experimental Trauma-Immunology, University Hospital Ulm, Ulm, Germany.
Alireza AbaeiCore Facility Small Animal Magnetic Resonance Imaging, Ulm University, Ulm, Germany.
Volker RascheCore Facility Small Animal Magnetic Resonance Imaging, Ulm University, Ulm, Germany.
Markus Huber-LangInstitute of Clinical and Experimental Trauma-Immunology, University Hospital Ulm, Ulm, Germany.
Bernd BaumannInstitute of Physiological Chemistry, Ulm University, Ulm, Germany.
Thomas WirthInstitute of Physiological Chemistry, Ulm University, Ulm, Germany.
Universität Ulm · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is the leading cause of death in young adults. After the initial injury, a poorly understood secondary phase, including a strong inflammatory response determines the final outcome of TBI. The inhibitor of NF-κB kinase (IKK)/NF-κB signaling system is the key regulator of inflammation and also critically involved in regulation of neuronal survival and synaptic plasticity. We addressed the neuron-specific function of IKK2/NF-κB signaling pathway in TBI using an experimental model of closed-head injury (CHI) in combination with mouse models allowing conditional regulation of IKK/NF-κB signaling in excitatory forebrain neurons. We found that repression of IKK2/NF-κB signaling in neurons increases the acute posttraumatic mortality rate, worsens the neurological outcome, and promotes neuronal cell death by apoptosis, thus resulting in enhanced proinflammatory gene expression. As a potential mechanism, we identified elevated levels of the proapoptotic mediators Bax and Bad and enhanced expression of stress response genes. This phenotype is also observed when neuronal IKK/NF-κB activity is inhibited just before CHI. In contrast, neuron-specific activation of IKK/NF-κB signaling does not alter the TBI outcome. Thus, this study demonstrates that physiological neuronal IKK/NF-κB signaling is necessary and sufficient to protect neurons from trauma consequences.-Mettang, M., Reichel, S. N., Lattke, M., Palmer, A., Abaei, A., Rasche, V., Huber-Lang, M., Baumann, B., Wirth, T. IKK2/NF-κB signaling protects neurons after traumatic brain injury.

Indexed as

AnimalsApoptosisBrain Injuries, TraumaticI-kappa B KinaseMiceNeuronsNF-kappa BSignal TransductionI-kappa B KinaseIkbkb protein, mouseNF-kappa Bapoptosis neurological outcomeconditional mouse modelneurodegenerationneuroinflammation

Identifiers

PMID29187362
PMCPMC5893169
OpenAlexW2768670265

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.