Evidence map›Paper›PMID 29115990›Full record

ArticleJournal of neuroinflammation2017

DHCR24 exerts neuroprotection upon inflammation-induced neuronal death.

Henna Martiskainen, Kaisa M A Paldanius, Teemu Natunen, Mari Takalo, Mikael Marttinen, Stina Leskelä, Nadine Huber, Petra Mäkinen, Enni Bertling, Hiramani Dhungana and 9 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

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  8. SDS3 regulates microglial inflammation by modulating the expression of the upstream kinase ASK1 in the p38 MAPK signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

19 authors at 2 institutions in 1 country.

Henna MartiskainenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Kaisa M A PaldaniusInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Teemu NatunenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Mari TakaloInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Mikael MarttinenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Stina LeskeläA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Nadine HuberA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Petra MäkinenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Enni BertlingMinerva Foundation Institute for Medical Research, Helsinki, Finland.
Hiramani DhunganaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Mikko HuuskonenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Paavo HonkakoskiSchool of Pharmacy, University of Eastern Finland, Kuopio, Finland.
Pirta HotulainenMinerva Foundation Institute for Medical Research, Helsinki, Finland.
Kirsi RillaInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Jari KoistinahoA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Hilkka SoininenInstitute of Clinical Medicine - Neurology, University of Eastern Finland, Kuopio, Finland.
Tarja MalmA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
Annakaisa HaapasaloA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland. annakaisa.haapasalo@uef.fi.
Mikko HiltunenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland. mikko.hiltunen@uef.fi.ORCID http://orcid.org/0000-0003-1508-4908
University of Eastern Finland · FIMinerva Foundation · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDHCR24, involved in the de novo synthesis of cholesterol and protection of neuronal cells against different stress conditions, has been shown to be selectively downregulated in neurons of the affected brain areas in Alzheimer's disease.

methodsHere, we investigated whether the overexpression of DHCR24 protects neurons against inflammation-induced neuronal death using co-cultures of mouse embryonic primary cortical neurons and BV2 microglial cells upon acute neuroinflammation. Moreover, the effects of DHCR24 overexpression on dendritic spine density and morphology in cultured mature mouse hippocampal neurons and on the outcome measures of ischemia-induced brain damage in vivo in mice were assessed.

resultsOverexpression of DHCR24 reduced the loss of neurons under inflammation elicited by LPS and IFN-γ treatment in co-cultures of mouse neurons and BV2 microglial cells but did not affect the production of neuroinflammatory mediators, total cellular cholesterol levels, or the activity of proteins linked with neuroprotective signaling. Conversely, the levels of post-synaptic cell adhesion protein neuroligin-1 were significantly increased upon the overexpression of DHCR24 in basal growth conditions. Augmentation of DHCR24 also increased the total number of dendritic spines and the proportion of mushroom spines in mature mouse hippocampal neurons. In vivo, overexpression of DHCR24 in striatum reduced the lesion size measured by MRI in a mouse model of transient focal ischemia.

conclusionsThese results suggest that the augmentation of DHCR24 levels provides neuroprotection in acute stress conditions, which lead to neuronal loss in vitro and in vivo.

Indexed as

AnimalsBrain IschemiaCell DeathCoculture TechniquesHippocampusHumansInflammationMaleMiceMicrogliaNeuronsNeuroprotectionOxidoreductases Acting on CH-CH Group DonorsOxidoreductases Acting on CH-CH Group DonorsAlzheimer’s diseaseDHCR24/Seladin-1NeuroinflammationNeuroprotection

Identifiers

PMID29115990
PMCPMC5678793
OpenAlexW2767903781

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.