Evidence map›Paper›PMID 27296697›Full record

ArticleMolecular and cellular biology2016

Gata3 Hypomorphic Mutant Mice Rescued with a Yeast Artificial Chromosome Transgene Suffer a Glomerular Mesangial Cell Defect.

Takashi Moriguchi, Lei Yu, Akihito Otsuki, Keiko Ainoya, Kim-Chew Lim, Masayuki Yamamoto, James Douglas Engel

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. 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
1.4field-weighted citation impact, top 18% 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, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. A Novel Role for GATA3 in Mesangial Cells in Glomerular Development and Injury.Journal of the American Society of Nephrology : JASN · 2019
    Article
  7. Article
  8. AMolecular and cellular biology · 2018
    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

7 authors at 2 institutions in 2 countries.

Takashi MoriguchiDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan moriguch@med.tohoku.ac.jp engel@umich.edu.
Lei YuDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Akihito OtsukiDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Keiko AinoyaDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Kim-Chew LimDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA.
Masayuki YamamotoDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
James Douglas EngelDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA moriguch@med.tohoku.ac.jp engel@umich.edu.
Tohoku University · JPUniversity of Michigan · US

Funding

GATA TRANSCRIPTION FACTOR FUNCTION IN DEVELOPMENTR01GM028896 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ENGEL, JAMES DOUGLAS · 1985 to 2004
$1.6M
NIGMS NIH HHS R01 GM028896
6 · The paper itself

Abstract

GATA3 is a zinc finger transcription factor that plays a crucial role in embryonic kidney development, while its precise functions in the adult kidney remain largely unexplored. Here, we demonstrate that GATA3 is specifically expressed in glomerular mesangial cells and plays a critical role in the maintenance of renal glomerular function. Newly generated Gata3 hypomorphic mutant mice exhibited neonatal lethality associated with severe renal hypoplasia. Normal kidney size was restored by breeding the hypomorphic mutant with a rescuing transgenic mouse line bearing a 662-kb Gata3 yeast artificial chromosome (YAC), and these animals (termed G3YR mice) survived to adulthood. However, most of the G3YR mice showed degenerative changes in glomerular mesangial cells, which deteriorated progressively during postnatal development. Consequently, the G3YR adult mice suffered severe renal failure. We found that the 662-kb Gata3 YAC transgene recapitulated Gata3 expression in the renal tubules but failed to direct sufficient GATA3 activity to mesangial cells. Renal glomeruli of the G3YR mice had significantly reduced amounts of platelet-derived growth factor receptor (PDGFR), which is known to participate in the development and maintenance of glomerular mesangial cells. These results demonstrate a critical role for GATA3 in the maintenance of mesangial cells and its absolute requirement for prevention of glomerular disease.

Indexed as

AnimalsChromosomes, Artificial, YeastDisease Models, AnimalGATA3 Transcription FactorGlomerular MesangiumKidney DiseasesKidney TubulesMiceMice, TransgenicPlatelet-Derived Growth FactorTransgenesGata3 protein, mouseGATA3 Transcription FactorPlatelet-Derived Growth Factor

Identifiers

PMID27296697
PMCPMC4985934
OpenAlexW2518654183

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.