Evidence map›Paper›PMID 17023583›Full record

ArticleBlood2007

Urea stimulation of KCl cotransport induces abnormal volume reduction in sickle reticulocytes.

Clinton H Joiner, R Kirk Rettig, Maorong Jiang, Mary Risinger, Robert S Franco

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Mechanosensitivity of wild-type and G551D cystic fibrosis transmembrane conductance regulator (CFTR) controls regulatory volume decrease in simple epithelia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  3. Pharmacological inhibition of calpain-1 prevents red cell dehydration and reduces Gardos channel activity in a mouse model of sickle cell disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  4. Article
  5. Article
  6. The emerging role of KCl cotransport in tumor biology.American journal of translational research · 2010
    Article
  7. Determinants of erythrocyte hydration.Current opinion in hematology · 2010
    Review
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Clinton H JoinerCincinnati Comprehensive Sickle Cell Center, Division of Hematology/Oncology, University of Cincinnati College of Medicine, and Department of Pediatrics, Cincinnati Children's Hospital Medical Center, OH 45229, USA. clinton.joiner@cchmc.org
R Kirk Rettig
Maorong Jiang
Mary Risinger
Robert S Franco
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Translational project: Gene therapy for Sickle Cell DiseaseU54HL070871 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI JOINER, CLINTON H · 2003 to 2011
$16.4M
NHLBI NIH HHS U54 HL070871
6 · The paper itself

Abstract

KCl cotransport (KCC) activity contributes to pathologic dehydration in sickle (SS) red blood cells (RBCs). KCC activation by urea was measured in SS and normal (AA) RBCs as Cl-dependent Rb influx. KCC-mediated volume reduction was assessed by measuring reticulocyte cellular hemoglobin concentration (CHC) cytometrically. Urea activated KCC fluxes in fresh RBCs to levels seen in swollen cells, although SS RBCs required lower urea concentrations than did normal (AA) RBCs. Little additional KCC stimulation by urea occurred in swollen AA or SS RBCs. The pH dependence of KCC in "euvolemic" SS RBCs treated with urea was similar to that in swollen cells. Urea triggered volume reduction in SS and AA reticulocytes, establishing a higher CHC. Volume reduction was Cl dependent and was limited by the KCC inhibitor, dihydro-indenyl-oxyalkanoic acid. Final CHC depended on urea concentration, but not on initial CHC. Under all activation conditions, volume reduction was exaggerated in SS reticulocytes and produced higher CHCs than in AA reticulocytes. The sulfhydryl-reducing agent, dithiothreitol, normalized the sensitivity of KCC activation to urea in SS RBCs and mitigated the urea-stimulated volume decrease in SS reticulocytes, suggesting that the dysfunctional activity of KCC in SS RBCs was due in part to reversible sulfhydryl oxidation.

Indexed as

Anemia, Sickle CellBiological TransportCell SizeDisulfidesDithiothreitolHemoglobinsHumansOxidation-ReductionPotassium ChlorideReticulocytesUreaDisulfidesDithiothreitolHemoglobinsPotassium ChlorideUrea

Identifiers

PMID17023583
PMCPMC1794068
OpenAlexW2078280187

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.