Evidence map›Paper›PMID 17167073›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2007

Endoplasmic reticulum stress exacerbates ischemia-reperfusion-induced apoptosis through attenuation of Akt protein synthesis in human choriocarcinoma cells.

Hong-wa Yung, Svitlana Korolchuk, Aviva M Tolkovsky, D Stephen Charnock-Jones, Graham J Burton

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing 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

60 citing papers in PubMed, 126 citations in OpenAlex.

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  10. Status of VEGF in preeclampsia and its effect on endoplasmic reticulum stress in placental trophoblast cells.European journal of obstetrics & gynecology and reproductive biology: X · 2019
    Article
  11. Noncanonical mitochondrial unfolded protein response impairs placental oxidative phosphorylation in early-onset preeclampsia.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Cell-Free DNA Release by Mouse Fetal Membranes.Reproductive sciences (Thousand Oaks, Calif.) · 2019
    Article
  13. Preeclampsia link to gestational hypoxia.Journal of developmental origins of health and disease · 2019
    Review
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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

5 authors at 1 institution in 1 country.

Hong-wa YungDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
Svitlana Korolchuk
Aviva M Tolkovsky
D Stephen Charnock-Jones
Graham J Burton
University of Cambridge · GB

Funding

Wellcome Trust 069027Wellcome Trust 069027/Z/02/Z
6 · The paper itself

Abstract

Oxidative stress is central to ischemia-reperfusion injury. The role of the endoplasmic reticulum (ER) in this process is uncertain. In ER signaling, PERK-Nrf2 and Ire-CHOP are two pathways that determine cell fate under stress. PERK-Nrf2 up-regulates antioxidant enzyme expression whereas Ire-CHOP promotes apoptosis. We have identified a novel pathway in ER stress-induced apoptosis after ischemia-reperfusion in vitro involving translational suppression of the survival kinase PKB/Akt (Akt), and elucidated an alternative protective role of antioxidants in the regulation of Akt activity. Using human choriocarcinoma JEG-3 cells, we found that sustained activation of ER stress by tunicamycin or thapsigargin exacerbated apoptosis in oxygen-glucose-deprived cells during reoxygenation. This was mediated via a reduction in phosphorylated Akt secondary to down-regulation of protein translation rather than suppression of phosphorylation. Transient overexpression of wild-type Akt, but not kinase-dead Akt, in JEG-3 cells diminished tunicamycin-OGD reoxygenation-induced apoptosis. The antioxidants Trolox and Edaravone reduced apoptosis, but the protective effect of Trolox was abrogated by the PI3K inhibitor, LY294002. We speculate that sustained ER stress may contribute to the placental dysfunction seen in human pregnancy complications.

Indexed as

ApoptosisChoriocarcinomaEndoplasmic ReticulumHumansIschemiaProto-Oncogene Proteins c-aktReperfusion InjuryStress, PhysiologicalTumor Cells, CulturedProto-Oncogene Proteins c-akt

Identifiers

PMID17167073
PMCPMC1885550
OpenAlexW2138664804

What OpenQuestion holds

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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.