Evidence map›Paper›PMID 24173102›Full record

ArticleAmerican journal of physiology. Cell physiology2014

Direct control of Na(+)-K(+)-2Cl(-)-cotransport protein (NKCC1) expression with aldosterone.

Bo Ding, Robert D Frisina, Xiaoxia Zhu, Yoshihisa Sakai, Bernd Sokolowski, Joseph P Walton

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  3. Article
  4. Dietary NaCellular and molecular life sciences : CMLS · 2023
    Article
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  6. Review
  7. Article
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  9. Review
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  11. Aldosterone up-regulates basolateral NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Review
  13. Article
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  15. 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

6 authors at 1 institution in 1 country.

Bo DingDepartment of Communication Sciences and Disorders, Global Center for Hearing and Speech Research, University of South Florida, Tampa, Florida;
Robert D Frisina
Xiaoxia Zhu
Yoshihisa Sakai
Bernd Sokolowski
Joseph P Walton
University of South Florida · US

Funding

Structure and Function Services CoreP01AG009524 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI FRISINA, ROBERT D · 1992 to 2021
$23.2M
DEVELOPMENT OF EXCITATION IN HAIR CELLSR01DC004295 · NIDCD · UNIVERSITY OF SOUTH FLORIDA · PI SOKOLOWSKI, BERND H · 2000 to 2015
$4.1M
NIA NIH HHS P01-AG-009524NIDCD NIH HHS R01 DC004295NIDCD NIH HHS R01-DC-004295
6 · The paper itself

Abstract

Sodium/potassium/chloride cotransporter (NKCC1) proteins play important roles in Na(+) and K(+) concentrations in key physiological systems, including cardiac, vascular, renal, nervous, and sensory systems. NKCC1 levels and functionality are altered in certain disease states, and tend to decline with age. A sensitive, effective way of regulating NKCC1 protein expression has significant biotherapeutic possibilities. The purpose of the present investigation was to determine if the naturally occurring hormone aldosterone (ALD) could regulate NKCC1 protein expression. Application of ALD to a human cell line (HT-29) revealed that ALD can regulate NKCC1 protein expression, quite sensitively and rapidly, independent of mRNA expression changes. Utilization of a specific inhibitor of mineralocorticoid receptors, eplerenone, implicated these receptors as part of the ALD mechanism of action. Further experiments with cycloheximide (protein synthesis inhibitor) and MG132 (proteasome inhibitor) revealed that ALD can upregulate NKCC1 by increasing protein stability, i.e., reducing ubiquitination of NKCC1. Having a procedure for controlling NKCC1 protein expression opens the doors for therapeutic interventions for diseases involving the mis-regulation or depletion of NKCC1 proteins, for example during aging.

Indexed as

Gene Expression RegulationAldosteroneHT29 CellsHumansProtein StabilityRNA, MessengerSolute Carrier Family 12, Member 2Up-RegulationAldosteroneRNA, MessengerSLC12A2 protein, humanSolute Carrier Family 12, Member 2agingNa+-K+-2Cl--cotransport proteinNKCC1pathway regulationphysiological systemssteroid hormonetherapeutics

Identifiers

PMID24173102
PMCPMC3919974
OpenAlexW2167979584

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.