Evidence map›Paper›PMID 24963280›Full record

ArticleExperimental neurobiology2014

Lipocalin-2 Acts as a Neuroinflammatogen in Lipopolysaccharide-injected Mice.

Myungwon Jin, Eunha Jang, Kyoungho Suk

Open access · bronzeAbstract read
In one paragraph

Article in Experimental neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

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  17. ASK1 signaling regulates phase-specific glial interactions during neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Review
  19. Lipocalin-2 and Cerebral Stroke.Frontiers in molecular neuroscience · 2022
    Review
  20. Novel therapeutic modulators of astrocytes for hydrocephalus.Frontiers in molecular neuroscience · 2022
    Review
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

3 authors at 1 institution in 1 country.

Myungwon JinDepartment of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, Daegu 700-422, Korea. ; Department of Biomedical Sciences, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu 700-422, Korea.
Eunha JangDepartment of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, Daegu 700-422, Korea. ; Department of Biomedical Sciences, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu 700-422, Korea.
Kyoungho SukDepartment of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, Daegu 700-422, Korea. ; Department of Biomedical Sciences, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu 700-422, Korea.
Kyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipocalin-2 (LCN2) is a key mediator of various cellular processes. Recent studies have indicated that LCN2 also plays an important role in central nervous system (CNS) injuries and neurological diseases, such as spinal cord injury, stroke, experimental autoimmune encephalomyelitis, and neurodegenerative diseases. Here, we investigated the role of LCN2 in a rodent model of lipopolysaccharide (LPS)-induced neuroinflammation. At 24 hours after intraperitoneal injection of LPS, LCN2 expression was strongly induced in the brain; LCN2 was mainly expressed in endothelial cells, astrocytes, and microglia. Next, we used LCN2-deficient mice to further investigate the role of LCN2 in neuroinflammation. LCN2 deficiency attenuated LPS-induced glial activation in the brain. In a mechanistic study employing glia/neuron co-cultures, LCN2 deficiency reduced glial neurotoxicity. Our results indicate that LCN2 plays a central role in the neuroinflammatory responses following LPS administration, and that LCN2 might contribute to the uncontrolled neurotoxic glial activation under excessive and chronic inflammatory conditions.

Indexed as

astrocytelipocalin-2neuroinflammationneuroinflammatogenneuron

Identifiers

PMID24963280
PMCPMC4065829
OpenAlexW2145538710

What OpenQuestion holds

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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.