Evidence map›Paper›PMID 28445976›Full record

ArticleOncotarget2017

Oxidative stress-induced apoptosis in granulosa cells involves JNK, p53 and Puma.

Hongyan Yang, Yan Xie, Dongyu Yang, Decheng Ren

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

119 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. SOD1 Overexpression Alleviates HAntioxidants (Basel, Switzerland) · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. NMN/NADJournal of ovarian research · 2026
    Article
  10. Article
  11. Oxidative Stress andInternational journal of molecular sciences · 2026
    Review
  12. Article
  13. The inflammatory clock: how cGAS-STING ticks in the aging ovary.Frontiers in cell and developmental biology · 2026
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

59 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Hongyan YangKey Research Laboratory of Gynecology, Department of Gynecology, The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Yuexiu District, Guangzhou, Guangdong 510120, China.
Yan XieKey Research Laboratory of Gynecology, Department of Gynecology, The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Yuexiu District, Guangzhou, Guangdong 510120, China.
Dongyu YangKey Research Laboratory of Gynecology, Department of Gynecology, The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Yuexiu District, Guangzhou, Guangdong 510120, China.
Decheng RenDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Guangdong Provincial Hospital of Traditional Chinese Medicine · CNGuangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) play important roles in follicular development and survival. Granulosa cell death is associated with increased ROS, but the mechanism of granulosa cell death induced by ROS is not clear. In order to define the molecular link between ROS and granulosa cell death, COV434, human granulosa tumor cells, were treated with H2O2. Compared to control cells, H2O2 induced granulosa cell death in a dose- and time-dependent manner. H2O2 induced an increase in Bax, Bak and Puma, and a decrease in anti-apoptotic molecules such as Bcl-2, Bcl-xL and Mcl-1. Both knockdown of Puma and overexpression of Bcl-xL could inhibit H2O2-induced granulosa cell death. These results suggest that suppression of Puma and overexpression of anti-apoptotic Bcl-2 family members could improve granulosa cell survival. To explore the mechanisms responsible for these findings, ROS in granulosa cells treatment with H2O2 were measured. The results showed that ROS was increased in a H2O2 dose- and time-dependent manner at the earlier time point. In addition, H2O2 induced an increase in Nrf2 and phosphorylation of JNK and p53. SP600125, an inhibitor of JNK, inhibits H2O2-induced phosphorylation of JNK and p53, and granulosa cell death. Antioxidant N-acetylcysteine (NAC) dose-dependently prevents H2O2-induced granulosa cell death. Furthermore, NAC also prevents phosphorylation of JNK and p53 induced by H2O2. Taken together, these data suggest that H2O2 regulates cell death in granulosa cells via the ROS-JNK-p53 pathway. These findings provide an improved understanding of the mechanisms underlying granulosa cell apoptosis, which could potentially be useful for future clinical applications.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCell LineFemaleGranulosa CellsHEK293 CellsHumansHydrogen PeroxideMAP Kinase Kinase 4MAP Kinase Signaling SystemMiceOxidative StressProto-Oncogene ProteinsReactive Oxygen SpeciesTumor Suppressor Protein p53Apoptosis Regulatory ProteinsBBC3 protein, humanHydrogen PeroxideMAP Kinase Kinase 4Proto-Oncogene ProteinsPUMA protein, mouseReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteinsgranulosa cell apoptosisH2O2JNKp53Puma

Identifiers

PMID28445976
PMCPMC5421932
OpenAlexW2591747488

What OpenQuestion holds

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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.