Evidence map›Paper›PMID 27591740›Full record

ArticleThe journal of gene medicine2016

A kidney injury molecule-1 (Kim-1) gene reporter in a mouse artificial chromosome: the responsiveness to cisplatin toxicity in immortalized mouse kidney S3 cells.

Kenji Kokura, Yasushi Kuromi, Takeshi Endo, Naohiko Anzai, Yasuhiro Kazuki, Mitsuo Oshimura, Tetsuya Ohbayashi

Open access · hybridAbstract read
In one paragraph

Article in The journal of gene medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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  7. Humanized UGT2 and CYP3A transchromosomic rats for improved prediction of human drug metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

7 authors at 2 institutions in 1 country.

Kenji KokuraChromosome Engineering Research Center (CERC), Tottori University, Tottori, Japan.ORCID http://orcid.org/0000-0001-6616-2270
Yasushi KuromiTottori Industrial Promotion Organization, Tottori, Tottori, Japan.
Takeshi EndoTottori Industrial Promotion Organization, Tottori, Tottori, Japan.
Naohiko AnzaiDepartment of Pharmacology and Toxicology, Dokkyo Medical University School of Medicine, Tochigi, Japan.
Yasuhiro KazukiChromosome Engineering Research Center (CERC), Tottori University, Tottori, Japan.
Mitsuo OshimuraChromosome Engineering Research Center (CERC), Tottori University, Tottori, Japan.
Tetsuya OhbayashiTottori Industrial Promotion Organization, Tottori, Tottori, Japan. ohbayashi@grape.med.tottori-u.ac.jp.
Tottori University · JPChiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKidney injury molecule-1 (Kim-1) has been validated as a urinary biomarker for acute and chronic renal damage. The expression of Kim-1 mRNA is also activated by acute kidney injury induced by cisplatin in rodents and humans. To date, the measurement of Kim-1 expression has not fully allowed the detection of in vitro cisplatin nephrotoxicity in immortalized culture cells, such as human kidney-2 cells and immortalized proximal tubular epithelial cells.

methodsWe measured the augmentation of Kim-1 mRNA expression after the addition of cisplatin using immortalized S3 cells established from the kidneys of transgenic mice harboring temperature-sensitive large T antigen from Simian virus 40.

resultsA mouse Kim-1 gene luciferase reporter in conjunction with an Hprt gene reporter detected cisplatin-induced nephrotoxicity in S3 cells. These two reporter genes were contained in a mouse artificial chromosome, and two luciferases that emitted different wavelengths were used to monitor the respective gene expression. However, the Kim-1 reporter gene failed to respond to cisplatin in A9 fibroblast cells that contained the same reporter mouse artificial chromosome, suggesting cell type-specificity for activation of the reporter.

conclusionsWe report the feasibility of measuring in vitro cisplatin nephrotoxicity using a Kim-1 reporter gene in S3 cells.

Indexed as

AnimalsAntineoplastic AgentsCell LineCell ProliferationChromosomes, ArtificialCisplatinFibroblastsGene Expression RegulationGenes, ReporterHepatitis A Virus Cellular Receptor 1Hypoxanthine PhosphoribosyltransferaseKidneyLuciferasesMice, TransgenicAntineoplastic AgentsCisplatinHavcr1 protein, mouseHepatitis A Virus Cellular Receptor 1Hypoxanthine PhosphoribosyltransferaseLuciferasescisplatinKim-1mouse artificial chromosomenephrotoxicityreporter geneS3 cells

Identifiers

PMID27591740
PMCPMC5095820
OpenAlexW2517401203

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.