Evidence map›Paper›PMID 27226632›Full record

ArticleThe Journal of biological chemistry2016

Dual Roles of Group IID Phospholipase A2 in Inflammation and Cancer.

Yoshimi Miki, Yuh Kidoguchi, Mariko Sato, Yoshitaka Taketomi, Choji Taya, Kazuaki Muramatsu, Michael H Gelb, Kei Yamamoto, Makoto Murakami

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 76 citations in OpenAlex.

  1. Trial
  2. Article
  3. The Phospholipase AJournal of lipid and atherosclerosis · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Secreted Phospholipases A2: Drivers of Inflammation and Cancer.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. The Roles of sPLABiomolecules · 2023
    Review
  18. Review
  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

9 authors at 4 institutions in 2 countries.

Yoshimi MikiFrom the Lipid Metabolism Project and.
Yuh KidoguchiFrom the Lipid Metabolism Project and the School of Science and Engineering, Tokyo Denki University, Saitama 350-0394, Japan.
Mariko SatoFrom the Lipid Metabolism Project and the School of Science and Engineering, Tokyo Denki University, Saitama 350-0394, Japan.
Yoshitaka TaketomiFrom the Lipid Metabolism Project and.
Choji TayaCenter for Basic Technology Research, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Kazuaki Muramatsuthe School of Science and Engineering, Tokyo Denki University, Saitama 350-0394, Japan.
Michael H Gelbthe Departments of Chemistry and Biochemistry, University of Washington, Seattle, Washington 98195.
Kei YamamotoFrom the Lipid Metabolism Project and the Faculty of Bioscience and Bioindustry, Tokushima University, Tokushima 770-8513, Japan, and PRIME and.
Makoto MurakamiFrom the Lipid Metabolism Project and AMED-CREST, Japan Agency for Medical Research and Development, Tokyo 100-0004, Japan murakami-mk@igakuken.or.jp.
Tokyo Metropolitan Institute of Medical Science · JPTokyo Denki University · JPJapan Agency for Medical Research and Development · JPUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phospholipase A2 enzymes have long been implicated in the promotion of inflammation by mobilizing pro-inflammatory lipid mediators, yet recent evidence suggests that they also contribute to anti-inflammatory or pro-resolving programs. Group IID-secreted phospholipase A2 (sPLA2-IID) is abundantly expressed in dendritic cells in lymphoid tissues and resolves the Th1 immune response by controlling the steady-state levels of anti-inflammatory lipids such as docosahexaenoic acid and its metabolites. Here, we show that psoriasis and contact dermatitis were exacerbated in Pla2g2d-null mice, whereas they were ameliorated in Pla2g2d-overexpressing transgenic mice, relative to littermate wild-type mice. These phenotypes were associated with concomitant alterations in the tissue levels of ω3 polyunsaturated fatty acid (PUFA) metabolites, which had the capacity to reduce the expression of pro-inflammatory and Th1/Th17-type cytokines in dendritic cells or lymph node cells. In the context of cancer, however, Pla2g2d deficiency resulted in marked attenuation of skin carcinogenesis, likely because of the augmented anti-tumor immunity. Altogether, these results underscore a general role of sPLA2-IID as an immunosuppressive sPLA2 that allows the microenvironmental lipid balance toward an anti-inflammatory state, exerting beneficial or detrimental impact depending upon distinct pathophysiological contexts in inflammation and cancer.

Indexed as

Immunity, CellularAnimalsFatty Acids, Omega-3Group II Phospholipases A2InflammationMiceMice, KnockoutNeoplasm ProteinsSkin NeoplasmsTh17 CellsTh1 CellsFatty Acids, Omega-3Group II Phospholipases A2Neoplasm ProteinsPla2g2d protein, mouse

Identifiers

PMID27226632
PMCPMC4957044
OpenAlexW2407281812

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.