Evidence map›Paper›PMID 25619259›Full record

ArticleImmunology2015

Salt-inducible kinase 3 deficiency exacerbates lipopolysaccharide-induced endotoxin shock accompanied by increased levels of pro-inflammatory molecules in mice.

Masato Sanosaka, Minoru Fujimoto, Tomoharu Ohkawara, Takahiro Nagatake, Yumi Itoh, Mai Kagawa, Ayako Kumagai, Hiroyuki Fuchino, Jun Kunisawa, Tetsuji Naka and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Manual Therapy Improves Fibromyalgia Symptoms by DownregulatingInternational journal of molecular sciences · 2024
    Observational
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Function and Transcriptional Regulation of BovineInternational journal of molecular sciences · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

11 authors at 1 institution in 1 country.

Masato SanosakaLaboratory of Cell Signalling and Metabolic Disease, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
Minoru Fujimoto
Tomoharu Ohkawara
Takahiro Nagatake
Yumi Itoh
Mai Kagawa
Ayako Kumagai
Hiroyuki Fuchino
Jun Kunisawa
Tetsuji Naka
Hiroshi Takemori
National Institute of Biomedical Innovation, Health and Nutrition · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages play important roles in the innate immune system during infection and systemic inflammation. When bacterial lipopolysaccharide (LPS) binds to Toll-like receptor 4 on macrophages, several signalling cascades co-operatively up-regulate gene expression of inflammatory molecules. The present study aimed to examine whether salt-inducible kinase [SIK, a member of the AMP-activated protein kinase (AMPK) family] could contribute to the regulation of immune signal not only in cultured macrophages, but also in vivo. LPS up-regulated SIK3 expression in murine RAW264.7 macrophages and exogenously over-expressed SIK3 negatively regulated the expression of inflammatory molecules [interleukin-6 (IL-6), nitric oxide (NO) and IL-12p40] in RAW264.7 macrophages. Conversely, these inflammatory molecule levels were up-regulated in SIK3-deficient thioglycollate-elicited peritoneal macrophages (TEPM), despite no impairment of the classical signalling cascades. Forced expression of SIK3 in SIK3-deficient TEPM suppressed the levels of the above-mentioned inflammatory molecules. LPS injection (10 mg/kg) led to the death of all SIK3-knockout (KO) mice within 48 hr after treatment, whereas only one mouse died in the SIK1-KO (n = 8), SIK2-KO (n = 9) and wild-type (n = 8 or 9) groups. In addition, SIK3-KO bone marrow transplantation increased LPS sensitivity of the recipient wild-type mice, which was accompanied by an increased level of circulating IL-6. These results suggest that SIK3 is a unique negative regulator that suppresses inflammatory molecule gene expression in LPS-stimulated macrophages.

Indexed as

AnimalsCell LineGene Expression RegulationInflammation MediatorsInterleukin-12 Subunit p40Interleukin-6LipopolysaccharidesMacrophages, PeritonealMiceMice, KnockoutNitric OxideProtein Serine-Threonine KinasesShock, SepticSignal TransductionInflammation MediatorsInterleukin-12 Subunit p40Interleukin-6LipopolysaccharidesNitric OxideProtein Serine-Threonine KinasesSIK3 protein, mouseAMP-activated protein kinaseendotoxin shockinducible nitric oxide synthaseinterleukin-12p40interleukin-1βinterleukin-6macrophagesalt-inducible kinasestumour necrosis factor-α

Identifiers

PMID25619259
PMCPMC4427391
OpenAlexW1803036946

What OpenQuestion holds

Textmetadata
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.