Evidence map›Paper›PMID 28750036›Full record

ArticlePloS one2017

Generation and phenotypic characterization of Pde1a mutant mice.

Xiaofang Wang, Satsuki Yamada, Wells B LaRiviere, Hong Ye, Jason L Bakeberg, María V Irazabal, Fouad T Chebib, Jan van Deursen, Peter C Harris, Caroline R Sussman and 3 more

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

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  15. Article
  16. Phosphodiesterases Expression during Murine Cardiac Development.International journal of molecular sciences · 2021
    Article
  17. Review
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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

13 authors.

Xiaofang WangDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Satsuki YamadaDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, United States of America.
Wells B LaRiviereDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Hong YeDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Jason L BakebergDivision of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
María V IrazabalDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Fouad T ChebibDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Jan van DeursenDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, United States of America.
Peter C HarrisDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Caroline R SussmanDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.
Atta BehfarDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, United States of America.
Christopher J WardDivision of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Vicente E TorresDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States of America.ORCID http://orcid.org/0000-0003-2008-1576

Funding

Pilot and FeasibilityP30DK090728 · NIDDK · MAYO CLINIC ROCHESTER · PI ROMERO, MICHAEL F. · 2010 to 2019
$11.8M
RENIN ANGIOTENSIN SYSTEM IN THE PATHOGENESIS OF ADPKDR01DK044863 · NIDDK · MAYO CLINIC ROCHESTER · PI TORRES, VICENTE E · 1991 to 2019
$4.5M
Novel treatment for polycystic kidney diseaseR56DK044863 · NIDDK · MAYO CLINIC ROCHESTER · PI TORRES, VICENTE E · 2015 to 2015
$119k
NIDDK NIH HHS P30 DK090728NIDDK NIH HHS R01 DK044863NIDDK NIH HHS R56 DK044863
6 · The paper itself

Abstract

It has been proposed that a reduction in intracellular calcium causes an increase in intracellular cAMP and PKA activity through stimulation of calcium inhibitable adenylyl cyclase 6 and inhibition of phosphodiesterase 1 (PDE1), the main enzymes generating and degrading cAMP in the distal nephron and collecting duct, thus contributing to the development and progression of autosomal dominant polycystic kidney disease (ADPKD). In zebrafish pde1a depletion aggravates and overexpression ameliorates the cystic phenotype. To study the role of PDE1A in a mammalian system, we used a TALEN pair to Pde1a exon 7, targeting the histidine-aspartic acid dipeptide involved in ligating the active site Zn++ ion to generate two Pde1a null mouse lines. Pde1a mutants had a mild renal cystic disease and a urine concentrating defect (associated with upregulation of PDE4 activity and decreased protein kinase A dependent phosphorylation of aquaporin-2) on a wild-type genetic background and aggravated renal cystic disease on a Pkd2WS25/- background. Pde1a mutants additionally had lower aortic blood pressure and increased left ventricular (LV) ejection fraction, without a change in LV mass index, consistent with the high aortic and low cardiac expression of Pde1a in wild-type mice. These results support an important role of PDE1A in the renal pathogenesis of ADPKD and in the regulation of blood pressure.

Indexed as

AnimalsBlood PressureBody WeightCardiovascular SystemCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 1Deamino Arginine VasopressinHomozygoteKidneyMiceMice, KnockoutMice, Mutant StrainsMyocardiumOrgan SizePhenotypePolycystic Kidney, Autosomal DominantCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 1Deamino Arginine VasopressinPde1A protein, mouseProliferating Cell Nuclear AntigenTranscription Activator-Like Effector Nucleases

Identifiers

PMID28750036
PMCPMC5531505

What OpenQuestion holds

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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.