Evidence map›Paper›PMID 15215185›Full record

ArticleThe American journal of pathology2004

Soluble receptor (DcR3) and cellular inhibitor of apoptosis-2 (cIAP-2) protect human cytotrophoblast cells against LIGHT-mediated apoptosis.

Ryan M Gill, Joan S Hunt

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Significance of increased expression of decoy receptor 3 in chronic liver disease.Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2009
    Article
  9. Article
  10. 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

2 authors at 1 institution in 1 country.

Ryan M GillDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160-7400, USA.
Joan S Hunt
University of Kansas Medical Center · US

Funding

UNDERSTANDING THE ROLE OF SMALL RNAS IN ARABIDOPSIS POLLEN DEVELOPMENTP20RR016475 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI AZUMA, MIZUKI · 2001 to 2011
$38.1M
UTERINE VASCULAR CHANGES &ANGIOGENESIS DURING IMPLANTATIONU54HD033994 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI TERRANOVA, PAUL FRANK · 2001 to 2005
$5.6M
DECIDUAL CELL/PLACENTAL INTERACTIONSR01HD024212 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HUNT, JOAN SHERAR · 1994 to 2007
$1.7M
TRANSCRIPTIONAL REGULATION OF GONADOTROPIN BETA SUBUNITS DURING DEVELOPMENTP30HD033994 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HUNT, JOAN SHERAR · 1996 to 2000
$445k
DECIDUAL CELL/PLACENTAL INTERACTIONSR29HD024212 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HUNT, JOAN SHERAR · 1989 to 1993
–
NCRR NIH HHS P20 RR 16475-01NICHD NIH HHS HD 24212NICHD NIH HHS HD 33994NICHD NIH HHS P30 HD033994NICHD NIH HHS R01 HD024212NICHD NIH HHS U54 HD033994
6 · The paper itself

Abstract

LIGHT (tumor necrosis factor superfamily 14) is among the powerful apoptosis-inducing cytokines synthesized in human placentas. Here, we investigated mechanisms protecting cytotrophoblast (CTB) cells from LIGHT-mediated apoptosis. Viability assays and caspase-3 immunoblots using recombinant LIGHT were done to establish that CTB cells purified from term placentas resist LIGHT-induced apoptosis. Although the cells were also resistant to killing by another placental cytokine, interferon-gamma (IFN-gamma), a combination of the two induced apoptosis. Killing was prevented by DcR3-Fc fragment but not control human-Fc fragment, showing that apoptosis occurs via the LIGHT pathway and that soluble receptors provide protection. Next, two cellular inhibitors of apoptosis expressed in CTB cells, cellular inhibitor of apoptosis (cIAP)-1 and cIAP-2, were investigated for protection. Cellular IAP-1 was unchanged after stimulation with LIGHT whereas cIAP-2 mRNA and protein were elevated. The increase was abrogated by treating CTB cells with LIGHT + IFN-gamma, implying a central role for cIAP-2 in preventing LIGHT-mediated apoptosis and an ability of IFN-gamma to overcome cIAP-2 protection. Definitive evidence was provided in experiments that showed that cIAP-2 anti-sense morpholinos permit LIGHT to induce apoptosis in HT-29 cells. In summary, the data are consistent with the postulate that placental CTB cells are protected from LIGHT-mediated apoptosis by both soluble receptor, DcR3, and cIAP-2.

Indexed as

ApoptosisCaspasesCell SurvivalDrug SynergismFemaleGene Expression RegulationHT29 CellsHumansInterferon-gammaMembrane ProteinsModels, BiologicalOligonucleotides, AntisensePeptide FragmentsPlacentaPregnancyProteinsCaspasesInterferon-gammaMembrane ProteinsOligonucleotides, AntisensePeptide FragmentsProteinsReceptors, Tumor Necrosis FactorRecombinant ProteinsRNA, MessengerTNFSF14 protein, humanTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14

Identifiers

PMID15215185
PMCPMC1618528
OpenAlexW2056028122

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.