Evidence map›Paper›PMID 17482574›Full record

ArticleBiochemical and biophysical research communications2007

Hypercholesterolemia suppresses Kir channels in porcine bone marrow progenitor cells in vivo.

Emile R Mohler, Yun Fang, Rebecca Gusic Shaffer, Jonni Moore, Robert L Wilensky, Michael Parmacek, Irena Levitan

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. A molecular switch controls the impact of cholesterol on a Kir channel.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Shear-Stress Sensitive Inwardly-Rectifying KCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019
    Article
  7. Article
  8. Article
  9. Cholesterol binding to ion channels.Frontiers in physiology · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. Cholesterol and ion channels.Sub-cellular biochemistry · 2010
    Review
  14. Direct regulation of prokaryotic Kir channel by cholesterol.The Journal of biological chemistry · 2009
    Article
  15. Review
  16. Identification of a C-terminus domain critical for the sensitivity of Kir2.1 to cholesterol.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  17. 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

7 authors at 1 institution in 1 country.

Emile R MohlerDepartment of Medicine, Cardiovascular Division, Section of Vascular Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. mohlere@uphs.upenn.edu
Yun Fang
Rebecca Gusic Shaffer
Jonni Moore
Robert L Wilensky
Michael Parmacek
Irena Levitan
University of Pennsylvania · US

Funding

Cholesterol Regulation of Endothelial K+ ChannelsR01HL073965 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LEVITAN, IRENA · 2004 to 2024
$7.3M
ORGANIZATION AND FUNCTIONS OF LIPID RAFTS IN SPERMATOZOAR01HD045664 · NICHD · CORNELL UNIVERSITY ITHACA · PI TRAVIS, ALEXANDER J · 2004 to 2008
$1.3M
NHLBI NIH HHS HL073965NHLBI NIH HHS R01 HL073965NICHD NIH HHS HD045664NICHD NIH HHS R01 HD045664
6 · The paper itself

Abstract

objectiveInwardly-rectifying K(+) (Kir) channels are responsible for maintaining membrane potentials in a variety of cell types including endothelial cells where they modulate endothelium-dependent vasorelaxation. The goal of this study is to determine the functional expression of Kir channels in porcine bone marrow-derived side population (BM-SP) cells that demonstrate phenotypes of endothelial progenitor cells (EPCs). We further asses the hypercholesterolemia sensitivity of Kir channels in BM-SP cells, which may play a key role in hypercholesterolemia-mediated regulation of EPCs.

methodsTo assess the effect of hypercholesterolemia on Kir channels in BM-SP, Kir currents were recorded in SP cells sorted from the bone marrow of healthy or hypercholesterolemic animals.

resultsWe found Kir channels constitute the major conductance in porcine bone marrow-derived side population (BM-SP) cells. These cells are defined by their efficiency of Hoechst dye efflux and have been reported to differentiate into multiple cell lineages including endothelium in vivo. We demonstrate here that porcine BM-SP cells differentiate to an endothelial lineage (CD31(+), vWF(+)) supporting the hypothesis that these cells are endothelial progenitor cells. Also, BM-SP cells express Kir with biophysical properties recapitulating those in mature endothelial cells, but with a much higher current density. Flow cytometric (FACS) analysis indicated that the number of SP cells was unaffected by hypercholesterolemia. However, hypercholesterolemia significantly inhibited Kir channels in BM-SP cells.

conclusionsWe successfully demonstrate that BM side population cells represent an origin of endothelial progenitor cells. This study further shows, for the fist time, that the functional expression of Kir channels in bone marrow (BM)-derived SP. Moreover, we demonstrate that hypercholesterolemia condition significantly suppresses the Kir channels in BM-SP cells, suggesting that hypercholesterolemia-mediated regulation of Kir channels may be an important factor not only in dysfunction of mature endothelium but also in dysfunction of BM-SP cells.

Indexed as

AnimalsBone Marrow CellsCell DifferentiationCell LineageCells, CulturedEndothelial CellsHypercholesterolemiaIn Vitro TechniquesMalePotassium Channels, Inwardly RectifyingStem CellsSwinePotassium Channels, Inwardly Rectifying

Identifiers

PMID17482574
PMCPMC2703014
OpenAlexW2169174941

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.