Evidence map›Paper›PMID 10597253›Full record

ArticleOncogene1999

The roles of caspase-3 and bcl-2 in chemically-induced apoptosis but not necrosis of renal epithelial cells.

Y Zhan, B van de Water, Y Wang, J L Stevens

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  13. Correlation of PDCD5 and apoptosis in hair cells and spiral ganglion neurons of different age of C57BL/6J mice.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2012
    Article
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  16. NADPH oxidase-1 plays a crucial role in hyperoxia-induced acute lung injury in mice.American journal of respiratory and critical care medicine · 2009
    Article
  17. Secondary necrosis in multicellular animals: an outcome of apoptosis with pathogenic implications.Apoptosis : an international journal on programmed cell death · 2008
    Review
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Y ZhanDepartment of Pathology, College of Medicine, University of Vermont, Burlington 05405, USA.
B van de Water
Y Wang
J L Stevens
Biomedical Research Institute · USAdirondack Medical Center · US

Funding

BIOCHEMICAL TOXICOLOGY AND MOLECULAR STRESS RESPONSESR01DK046267 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI ICHIMURA, TAKAHARU · 1994 to 2004
$1.4M
MOLECULAR TOXICOLOGY GENE EXPRESSION AND CELL DEATHR01ES007847 · NIEHS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI STEVENS, JAMES L. · 1996 to 1999
–
NIDDK NIH HHS DK46267NIEHS NIH HHS ES07847
6 · The paper itself

Abstract

The kidney is a target for toxicants including cisplatin and S-(1,2-dichlorovinyl)-L-cysteine (DCVC), a metabolite of the environmental contaminant, trichloroethylene. Necrosis is well characterized in kidney cells, but pathways leading to apoptosis are less clear. Cysteine conjugates are useful toxicants because they induce either necrosis or apoptosis depending on chemical structure or antioxidant status. Herein, we show that in the renal epithelial cell line LLC-PK1, activation of caspase-3 (CPP32/Yama/apopain) is crucial for apoptosis, but not necrosis. Apoptosis was blocked by zVAD.fmk, and partially by a cathepsin inhibitor. Caspase-3 activity and cleavage of poly(ADP-ribose) polymerase (PARP) was detected only during apoptosis. S-(1,1,2,2-Tetrafluoroethyl)-L-cysteine (TFEC), a metabolite of tetrafluoroethylene, kills cells only by necrosis, and did not activate caspases under any conditions. Apoptosis and activation of caspase-3 by cisplatin, but not DCVC, was prevented by bcl-2. Thus, caspase-3 activation by bcl-2-dependent and -independent mechanisms is a terminal event in chemical-apoptosis of renal epithelial cells.

Indexed as

AnimalsApoptosisCaspase 3CaspasesCisplatinEnzyme ActivationEpithelial CellsKidneyLLC-PK1 CellsNecrosisProtease InhibitorsProto-Oncogene Proteins c-bcl-2Signal TransductionSwineCaspase 3CaspasesCisplatinProtease InhibitorsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID10597253
OpenAlexW2019617863

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.