Evidence map›Paper›PMID 33542431›Full record

ArticleScientific reports2021

Genetic background-dependent abnormalities of the enteric nervous system and intestinal function in Kif26a-deficient mice.

Yukiko Ohara, Lisa Fujimura, Akemi Sakamoto, Youichi Teratake, Shuichi Hiraoka, Haruhiko Koseki, Takeshi Saito, Keita Terui, Tetsuya Mitsunaga, Mitsuyuki Nakata and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Yukiko OharaDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Lisa FujimuraBiomedical Research Center, Chiba University, Chiba, Japan.
Akemi SakamotoBiomedical Research Center, Chiba University, Chiba, Japan.
Youichi TeratakeBiomedical Research Center, Chiba University, Chiba, Japan.
Shuichi HiraokaLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences (RIKEN-IMS), Yokohama, Japan.
Haruhiko KosekiLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences (RIKEN-IMS), Yokohama, Japan.
Takeshi SaitoDepartment of Pediatric Surgery, Chiba Children's Hospital, Chiba, Japan.
Keita TeruiDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0003-4315-5179
Tetsuya MitsunagaDepartment of Pediatric Surgery, Chiba Children's Hospital, Chiba, Japan.
Mitsuyuki NakataDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hideo YoshidaDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Masahiko HatanoBiomedical Research Center, Chiba University, Chiba, Japan. hatanom@faculty.chiba-u.jp.
Chiba University · JPChiba Hospital · JPChiba University Hospital · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Kif26a protein-coding gene has been identified as a negative regulator of the GDNF-Ret signaling pathway in enteric neurons. The aim of this study was to investigate the influence of genetic background on the phenotype of Kif26a-deficient (KO, -/-) mice. KO mice with both C57BL/6 and BALB/c genetic backgrounds were established. Survival rates and megacolon development were compared between these two strains of KO mice. Functional bowel assessments and enteric neuron histopathology were performed in the deficient mice. KO mice with the BALB/c genetic background survived more than 400 days without evidence of megacolon, while all C57BL/6 KO mice developed megacolon and died within 30 days. Local enteric neuron hyperplasia in the colon and functional bowel abnormalities were observed in BALB/c KO mice. These results indicated that megacolon and enteric neuron hyperplasia in KO mice are influenced by the genetic background. BALB/c KO mice may represent a viable model for functional gastrointestinal diseases such as chronic constipation, facilitating studies on the underlying mechanisms and providing a foundation for the development of treatments.

Indexed as

AnimalsEnteric Nervous SystemGene Expression RegulationGlial Cell Line-Derived Neurotrophic FactorIntestine, SmallKinesinsMegacolonMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNADPH DehydrogenaseNeuronsProto-Oncogene Proteins c-retSignal TransductionSpecies SpecificityGdnf protein, mouseGlial Cell Line-Derived Neurotrophic FactorKinesinsNADPH DehydrogenaseProto-Oncogene Proteins c-retRet protein, mouse

Identifiers

PMID33542431
PMCPMC7862435
OpenAlexW3126824016

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Registered trials

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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.