Evidence map›Paper›PMID 28478097›Full record

ArticleDevelopmental biology2017

Non-muscle myosin II deletion in the developing kidney causes ureter-bladder misconnection and apical extrusion of the nephric duct lineage epithelia.

Fahim Haque, Yusuke Kaku, Sayoko Fujimura, Tomoko Ohmori, Robert S Adelstein, Ryuichi Nishinakamura

Abstract read
In one paragraph

Article in Developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Clinical and Genome-Wide Analysis of Serum Platinum Levels after Cisplatin-Based Chemotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 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

6 authors at 3 institutions in 2 countries.

Fahim HaqueDepartment of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Yusuke KakuDepartment of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Sayoko FujimuraLiaison Laboratory Research Promotion Center, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Tomoko OhmoriDepartment of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Robert S AdelsteinLaboratory of Molecular Cardiology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Ryuichi NishinakamuraDepartment of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan. Electronic address: ryuichi@kumamoto-u.ac.jp.
Kumamoto University · JPKumamoto Industrial Research Institute · JPNational Institutes of Health · US

Funding

The Role of Nonmuscle Myosins in Development and DiseaseZIAHL004223 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ADELSTEIN, ROBERT · 2009 to 2020
$7.1M
In Vivo Function of Nonmuscle Myosin II-AZIAHL004218 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ADELSTEIN, ROBERT · 2009 to 2019
$5.1M
Intramural NIH HHS ZIA HL004218
6 · The paper itself

Abstract

In kidney development, connection of the nephric duct (ND) to the cloaca and subsequent sprouting of the ureteric bud (UB) from the ND are important for urinary exit tract formation. Although the roles of Ret signaling are well established, it remains unclear how intracellular cytoskeletal proteins regulate these morphogenetic processes. Myh9 and Myh10 encode two different non-muscle myosin II heavy chains, and Myh9 mutations in humans are implicated in congenital kidney diseases. Here we report that ND/UB lineage-specific deletion of Myh9/Myh10 in mice caused severe hydroureter/hydronephrosis at birth. At mid-gestation, the mutant ND/UB epithelia exhibited aberrant basal protrusion and ectopic UB formation, which likely led to misconnection of the ureter to the bladder. In addition, the mutant epithelia exhibited apical extrusion followed by massive apoptosis in the lumen, which could be explained by reduced apical constriction and intercellular adhesion mediated by E-cadherin. These phenotypes were not ameliorated by genetic reduction of the tyrosine kinase receptor Ret. In contrast, ERK was activated in the mutant cells and its chemical inhibition partially ameliorated the phenotypes. Thus, myosin II is essential for maintaining the apicobasal integrity of the developing kidney epithelia independently of Ret signaling.

Indexed as

AnimalsAnimals, NewbornDogsEpitheliumGene Expression Regulation, DevelopmentalImmunohistochemistryIn Situ HybridizationKidneyMadin Darby Canine Kidney CellsMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, ConfocalMyosin Heavy ChainsNephronsNonmuscle Myosin Type IIAMyh9 protein, mouseMyosin Heavy ChainsNonmuscle Myosin Type IIANonmuscle Myosin Type IIBnonmuscle myosin type IIB heavy chainProto-Oncogene Proteins c-retRet protein, mouse

Identifiers

PMID28478097
PMCPMC6447305
OpenAlexW2611002644

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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.