Evidence map›Paper›PMID 28927423›Full record

ArticleJournal of neuroinflammation2017

Primary cilia modulate TLR4-mediated inflammatory responses in hippocampal neurons.

Hyunjung Baek, Hyo Jung Shin, Jwa-Jin Kim, Nara Shin, Sena Kim, Min-Hee Yi, Enji Zhang, Jinpyo Hong, Joon Won Kang, Yonghyun Kim and 2 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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
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  10. Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025
    Review
  11. Review
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  14. Review
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  17. Review
  18. ALS-linked C9orf72-SMCR8 complex is a negative regulator of primary ciliogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article
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

12 authors at 3 institutions in 3 countries.

Hyunjung BaekDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Hyo Jung ShinDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Jwa-Jin KimDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Nara ShinDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Sena KimDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Min-Hee YiDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Enji ZhangDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Jinpyo HongDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Joon Won KangDepartment of Pediatrics, Chungnam National University Hospital, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Yonghyun KimDepartment of Chemical and Biological Engineering, The University of Alabama, Tuscaloosa, AL, 35487, USA.
Cuk-Seong KimDepartment of Physiology, Department of Medical Science, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea. cskim@cnu.ac.kr.
Dong Woon KimDepartment of Anatomy, Department of Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea. vinsnu528@cnu.ac.kr.ORCID http://orcid.org/0000-0001-7691-1394
Chungnam National University · KRChungnam National University Hospital · KRUniversity of Alabama · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe primary cilium is an organelle that can act as a master regulator of cellular signaling. Despite the presence of primary cilia in hippocampal neurons, their function is not fully understood. Recent studies have demonstrated that the primary cilium influences interleukin (IL)-1β-induced NF-κB signaling, ultimately mediating the inflammatory response. We, therefore, investigated ciliary function and NF-κB signaling in lipopolysaccharide (LPS)-induced neuroinflammation in conjunction with ciliary length analysis.

methodsSince TLR4/NF-κB signaling is a well-known inflammatory pathway, we measured ciliary length and inflammatory mediators in wild type (WT) and TLR4

resultsPrimary ciliary length decreased in hippocampal pyramidal neurons after intracerebroventricular injection of LPS in WT mice, whereas it increased in TLR4

conclusionsThese data suggest that LPS-induced NF-κB signaling and inflammatory mediator expression are modulated by cilia and that the blockade of primary cilium formation by Kif3a siRNA regulates TLR4-induced NF-κB signaling. We propose that primary cilia are critical for regulating NF-κB signaling events in neuroinflammation and in the innate immune response.

Indexed as

AnimalsCiliaHippocampusInflammationMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsNF-kappa BSignal TransductionToll-Like Receptor 4NF-kappa BTlr4 protein, mouseToll-Like Receptor 4HippocampusNeuroinflammationNFκbPrimary ciliaTLR4

Identifiers

PMID28927423
PMCPMC5606072
OpenAlexW2755666968

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.