Evidence map›Paper›PMID 18718914›Full record

ArticleThe Journal of biological chemistry2008

15-deoxy-Delta(12,14)-prostaglandin J2 induces vascular endothelial cell apoptosis through the sequential activation of MAPKS and p53.

Tsung-Chuan Ho, Show-Li Chen, Yuh-Cheng Yang, Chia-Yi Chen, Fang-Ping Feng, Jui-Wen Hsieh, Huey-Chuan Cheng, Yeou-Ping Tsao

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Induction of Heme Oxygenase-1 by 15d-Prostaglandin JAntioxidants (Basel, Switzerland) · 2022
    Article
  3. Article
  4. Article
  5. 15-Deoxy-∆-PPAR research · 2019
    Review
  6. 15-Deoxy-ΔDrug design, development and therapy · 2019
    Review
  7. 15d-PGJ2 is a new hope for controlling tumor growth.American journal of translational research · 2018
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
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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

8 authors at 4 institutions in 1 country.

Tsung-Chuan HoDepartment of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan.
Show-Li Chen
Yuh-Cheng Yang
Chia-Yi Chen
Fang-Ping Feng
Jui-Wen Hsieh
Huey-Chuan Cheng
Yeou-Ping Tsao
National Defense Medical Center · TWMackay Memorial Hospital · TWNational Taiwan University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) is a potent anti-angiogenic factor and induces endothelial cell apoptosis, although the mechanism remains unclear. In this study, 15d-PGJ(2) was found to increase p53 levels of the human umbilical vein endothelial cells by stabilizing p53. Both 15d-PGJ(2)-induced apoptosis and the induction of p21(Waf1) and Bax can be abolished by p53 small interfering RNA but not by peroxisome proliferator-activated receptor gamma inhibitors. Moreover, 15d-PGJ(2) activated JNK and p38 MAPK while inducing p53 phosphorylation at sites responsible for p53 activity. JNK inhibitor (SP600125) or p38 MAPK inhibitor (SB203580) pretreatment attenuated 15d-PGJ(2)-mediated apoptosis and suppressed the p21(Waf1) and Bax expressions without affecting p53 protein accumulation. Pretreatment with SP600125 partially prevented the phosphorylation of p53 at serines 33 and 392 induced by 15d-PGJ(2). 15d-PGJ(2) was also found to induce reactive oxygen species generation and partially blocked nuclear factor-kappaB activity. Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2). Using a mouse model of corneal neovascularization, it was demonstrated in vivo that 15d-PGJ(2) induced reactive oxygen species generation, activated JNK and p38 MAPK, induced p53 accumulation/phosphorylation, and induced vascular endothelial cell apoptosis, which could be abolished by N-acetylcysteine, SP600125, SB203580, or a virus-derived amphipathic peptides-based p53 small interfering RNA. This is the first study that 15d-PGJ(2) induces vascular endothelial cell apoptosis through the signaling of JNK and p38 MAPK-mediated p53 activation both in vitro and in vivo, further establishing the potential of 15d-PGJ(2) as an anti-angiogenesis agent.

Indexed as

ApoptosisMAP Kinase Signaling SystemAnimalsDose-Response Relationship, DrugEndothelium, VascularEnzyme ActivationHumansMiceMice, Inbred BALB CModels, BiologicalNF-kappa BPhosphorylationProstaglandin D2Reactive Oxygen SpeciesTumor Suppressor Protein p5315-deoxy-delta(12,14)-prostaglandin J2NF-kappa BProstaglandin D2Reactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID18718914
PMCPMC2662083
OpenAlexW2045607632

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.