Evidence map›Paper›PMID 18650792›Full record

ArticleKidney international2008

Downregulation of Spry-1, an inhibitor of GDNF/Ret, causes angiotensin II-induced ureteric bud branching.

Ihor V Yosypiv, Mary K Boh, Melissa A Spera, Samir S El-Dahr

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Adhesion GPCRs in Kidney Development and Disease.Frontiers in cell and developmental biology · 2018
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Genetics of congenital anomalies of the kidney and urinary tract.Pediatric nephrology (Berlin, Germany) · 2011
    Review
  12. Receptor tyrosine kinases in kidney development.Journal of signal transduction · 2011
    Article
  13. Article
  14. Article
  15. Angiotensin II AT2 receptor regulates ureteric bud morphogenesis.American journal of physiology. Renal physiology · 2010
    Article
  16. Review
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Ihor V YosypivSection of Pediatric Nephrology, Department of Pediatrics, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA. iiosipi@tulane.edu
Mary K Boh
Melissa A Spera
Samir S El-Dahr
Tulane University · US

Funding

TULANE COBRE: TRANSGENIC &GENE-TARGETED ANIMAL COREP20RR017659 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PRIETO, MINOLFA C · 2002 to 2011
$22.1M
Inducible Dysplastic Nephropathy in B2-Deficient MiceR01DK056264 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI EL-DAHR, SAMIR S · 2000 to 2014
$3.8M
TERMINAL DIFFERENTIATION OF THE RENAL EPITHELIUMR01DK062250 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI EL-DAHR, SAMIR S · 2003 to 2012
$2.5M
Renin-ANG System in Morphogenesis of Renal MedullaR01DK071699 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI YOSYPIV, IHOR V · 2007 to 2011
$1.4M
NCRR NIH HHS P20 RR017659NCRR NIH HHS P20 RR17659NIDDK NIH HHS DK-56264NIDDK NIH HHS DK-62250NIDDK NIH HHS DK-71699NIDDK NIH HHS R01 DK056264NIDDK NIH HHS R01 DK062250NIDDK NIH HHS R01 DK071699
6 · The paper itself

Abstract

Mutations of genes in the renin-angiotensin system are associated with congenital abnormalities of the kidney and urinary tract. The major signaling pathway for branching morphogenesis during kidney development is the c-Ret receptor tyrosine kinase whose ligand is GDNF and whose downstream target is Wnt11. We determined whether angiotensin II, an inducer of ureteric bud branching in vitro, influences the GDNF/c-Ret/Wnt11 pathway. Mouse metanephroi were grown in the presence or absence of angiotensin II or an angiotensin type 1 receptor (AT1R) antagonist and gene expression was measured by whole mount in situ hybridization. Angiotensin II induced the expression of c-Ret and Wnt11 in ureteric bud tip cells. GDNF, a Wnt11-regulated gene expressed in the mesenchyme, was also upregulated by angiotensin II but this downregulated Spry1, an endogenous inhibitor of Ret tyrosine kinase activity in an AT1R-dependent manner. Angiotensin II also decreased Spry1 mRNA levels in cultured ureteric bud cells. Exogenous angiotensin II preferentially stimulated ureteric bud tip cell proliferation in vivo while AT1R blockade increased cell apoptosis. Our findings suggest AT1R-mediated inhibition of the Spry1 gene increases c-Ret tyrosine kinase activity leading to upregulation of its downstream target Wnt11. Enhanced Wnt11 expression induces GDNF in adjacent mesenchyme causing focal bursts of ureteric bud tip cell proliferation, decreased tip cell apoptosis and branching.

Indexed as

MorphogenesisAdaptor Proteins, Signal TransducingAngiotensin IIAnimalsApoptosisCell ProliferationDown-RegulationGene Expression RegulationGlial Cell Line-Derived Neurotrophic FactorGlial Cell Line-Derived Neurotrophic Factor ReceptorsKidneyMembrane ProteinsMesodermMicePhosphoproteinsReceptor, Angiotensin, Type 1Adaptor Proteins, Signal TransducingAngiotensin IIGlial Cell Line-Derived Neurotrophic FactorGlial Cell Line-Derived Neurotrophic Factor ReceptorsMembrane ProteinsPhosphoproteinsReceptor, Angiotensin, Type 1Spry1 protein, mouseWnt11 protein, mouseWnt Proteins

Identifiers

PMID18650792
PMCPMC2738599
OpenAlexW2069564382

What OpenQuestion holds

Textmetadata
LicenceTDM
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.