Evidence map›Paper›PMID 11849312›Full record

ArticleImmunology2002

Prostaglandin D(2), its metabolite 15-d-PGJ(2), and peroxisome proliferator activated receptor-gamma agonists induce apoptosis in transformed, but not normal, human T lineage cells.

Sarah G Harris, Richard P Phipps

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Exploring the nexus of nuclear receptors in hematological malignancies.Cellular and molecular life sciences : CMLS · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. The expansive role of oxylipins on platelet biology.Journal of molecular medicine (Berlin, Germany) · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Peroxisome proliferator-activated receptor gamma overexpression suppresses growth and induces apoptosis in human multiple myeloma cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sarah G HarrisDepartment of Microbiology and Immunology and the James P. Wilmot Cancer Center, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Richard P Phipps
University of Rochester · US

Funding

REGULATION OF IMMUNITY BY PROSTAGLANDINSR01DE011390 · NIDCR · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 1994 to 2009
$2.7M
CD40 AND LUNG INFLAMMATION AND FIBROSISR01HL056002 · NHLBI · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 1997 to 2000
$229k
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL007216 · NHLBI · UNIVERSITY OF ROCHESTER · PI HYDE, RICHARD W · 1985 to 2000
$53k
NHLBI NIH HHS HL007216NHLBI NIH HHS HL56002NHLBI NIH HHS T32 HL007216NIDCR NIH HHS DE11390NIDCR NIH HHS R01 DE011390
6 · The paper itself

Abstract

Prostaglandin D(2) (PGD(2)) is abundantly produced by mast cells, platelets, and alveolar macrophages and has been proposed as a key immunoregulatory lipid mediator. 15-Deoxy-Delta(12,14)-PGJ(2) (15-d-PGJ(2)), a key PGD(2) metabolite, is under intense study as a potential anti-inflammatory mediator. Little is known about PGD(2) or the role of 15-d-PGJ(2), if any, in regulating the activities of human T lineage cells. In this report we demonstrate that both PGD(2) and 15-d-PGJ(2) have potent antiproliferative effects, and in fact kill human T lymphocyte lines derived from malignant cells by an apoptotic mechanism. Interestingly, normal human T cells were not similarly affected. Although the T lymphocyte lines express mRNA for the PGD(2) receptor (DP-R), a potent DP receptor agonist, BW245C, did not inhibit the proliferation or viability of the cells, suggesting an alternative mechanism of action. PGD(2) and 15-d-PGJ(2) can bind to the peroxisome proliferator activated receptor-gamma (PPAR-gamma) which is implicated in lipid metabolism and apoptosis. Exposure to synthetic PPAR-gamma ligands (e.g. ciglitazone, troglitazone) mimicked the inhibitory responses of PGD(2) and 15-d-PGJ(2), and induced apoptosis in the transformed T cells consistent with a PPAR-gamma-dependent mechanism. These observations suggest that PPAR-gamma ligands (which may include PGD2) provide strong apoptotic signals to transformed, but not normal T lymphocytes. Thus, the efficacy of utilizing PPAR-gamma and its ligands as therapeutics for human T cell cancers needs to be further evaluated.

Indexed as

ThiazolidinedionesAntineoplastic AgentsApoptosisCell DivisionCell Line, TransformedCells, CulturedCell SurvivalChromansHumansHydantoinsIn Situ Nick-End LabelingProstaglandin D2Receptors, Cytoplasmic and NuclearReverse Transcriptase Polymerase Chain ReactionThiazolesT-Lymphocytes15-deoxy-delta(12,14)-prostaglandin J23-((2-cyclohexyl-2-hydroxyethylidene)amino)-2,5-dioxo-4-imidazolidineheptanoic acidAntineoplastic AgentsChromansHydantoinsProstaglandin D2Receptors, Cytoplasmic and NuclearThiazolesThiazolidinedionesTranscription FactorsTroglitazone

Identifiers

PMID11849312
PMCPMC1782633
OpenAlexW1973632746

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.