Evidence map›Paper›PMID 25294233›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Reduction in maternal circulating ouabain impairs offspring growth and kidney development.

Moran Dvela-Levitt, Hagit Cohen-Ben Ami, Haim Rosen, Asher Ornoy, Drorith Hochner-Celnikier, Menachem Granat, David Lichtstein

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024
    Review
  4. Review
  5. Article
  6. Endogenous Cardiac Steroids in Bipolar Disorder: State of the Art.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Role of endogenous ouabain in the etiology of bipolar disorder.International journal of bipolar disorders · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Ouabain-regulated phosphoproteome reveals molecular mechanisms for NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  13. Review
  14. Article
  15. Review
  16. Na⁺, K⁺-ATPase Signaling and Bipolar Disorder.International journal of molecular sciences · 2018
    Review
  17. Isoform-specific role of Na/K-ATPase α1 in skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2018
    Article
  18. Review
  19. Review
  20. Review
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.

Moran Dvela-LevittDepartments of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Hagit Cohen-Ben AmiDepartments of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Haim RosenMicrobiology and Molecular Genetics, and Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Asher OrnoyDepartments of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Drorith Hochner-CelnikierObstetrics and Gynecology.
Menachem GranatObstetrics and Gynecology.
David LichtsteinDepartments of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel davidli@ekmd.huji.ac.il.
Institute of Neurobiology · BGBeijing Obstetrics and Gynecology Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ouabain, a steroid present in the circulation and in various tissues, was shown to affect the growth and viability of various cells in culture. To test for the possible influence of this steroid on growth and viability in vivo, we investigated the involvement of maternal circulating ouabain in the regulation of fetal growth and organ development. We show that intraperitoneal administration of anti-ouabain antibodies to pregnant mice resulted in a >80% decline in the circulating ouabain level. This reduction caused a significant decrease in offspring body weight, accompanied by enlargement of the offspring heart and inhibition of kidney and liver growth. Kidney growth inhibition was manifested by a decrease in the size and number of nephrons. After the reduction in maternal circulating ouabain, kidney expression of cyclin D1 was reduced and the expression of the α1 isoform of the Na(+), K(+)-ATPase was increased. In addition, the elevation of proliferation signals including ERK1/2, p-90RSK, Akt, PCNA, and Ki-67, and a reduction in apoptotic factors such as Bax, caspase-3, and TUNEL were detected. During human pregnancy, the circulating maternal ouabain level increased and the highest concentration of the steroid was found in the placenta. Furthermore, circulating ouabain levels in women with small-for-gestational age neonates were significantly lower than the levels in women with normal-for-gestational age newborns. These results support the notion that ouabain is a growth factor and suggest that a reduction in the concentration of this hormone during pregnancy may increase the risk of impaired growth and kidney development.

Indexed as

AnimalsBody WeightCell ProliferationCell SurvivalFemaleHumansInfant, NewbornInfant, Small for Gestational AgeKidneyMice, Inbred ICROrgan SizeOuabainPregnancyOuabaincardiac steroidsdevelopmentendogenous ouabaingrowthK+-ATPasekidneyNa+signaling

Identifiers

PMID25294233
PMCPMC4413757
OpenAlexW2011928404

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.