Evidence map›Paper›PMID 12496090›Full record

ArticleBiophysical journal2002

Modulation of endothelial inward-rectifier K+ current by optical isomers of cholesterol.

Victor G Romanenko, George H Rothblat, Irena Levitan

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Biophysical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

93 citing papers in PubMed, 189 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Cholesterol regulation of mechanosensitive ion channels.Frontiers in cell and developmental biology · 2024
    Review
  8. Endothelial KAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  9. Review
  10. Review
  11. Review
  12. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  13. Article
  14. Article
  15. 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
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

33 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Victor G RomanenkoInstitute for Medicine and Engineering, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
George H Rothblat
Irena Levitan
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

Cell and molecular studies in cardiovascular engineeringR01HL064388 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DAVIES, PETER FRANCIS · 2001 to 2005
$6.9M
NHLBI NIH HHS R01 HL 64388-01A1
6 · The paper itself

Abstract

Membrane potential of aortic endothelial cells under resting conditions is dominated by inward-rectifier K(+) channels belonging to the Kir 2 family. Regulation of endothelial Kir by membrane cholesterol was studied in bovine aortic endothelial cells by altering the sterol composition of the cell membrane. Our results show that enriching the cells with cholesterol decreases the Kir current density, whereas depleting the cells of cholesterol increases the density of the current. The dependence of the Kir current density on the level of cellular cholesterol fits a sigmoid curve with the highest sensitivity of the Kir current at normal physiological levels of cholesterol. To investigate the mechanism of Kir regulation by cholesterol, endogenous cholesterol was substituted by its optical isomer, epicholesterol. Substitution of approximately 50% of cholesterol by epicholesterol results in an early and significant increase in the Kir current density. Furthermore, substitution of cholesterol by epicholesterol has a stronger facilitative effect on the current than cholesterol depletion. Neither single channel properties nor membrane capacitance were significantly affected by the changes in the membrane sterol composition. These results suggest that 1) cholesterol modulates cellular K(+) conductance by changing the number of the active channels and 2) that specific cholesterol-protein interactions are critical for the regulation of endothelial Kir.

Indexed as

beta-CyclodextrinsAnimalsAortaCattleCells, CulturedCholesterolCyclodextrinsDose-Response Relationship, DrugEndothelium, VascularIon Channel GatingMembrane PotentialsPotassium Channels, Inwardly RectifyingReference ValuesReproducibility of ResultsSensitivity and SpecificityStereoisomerismbeta-CyclodextrinsCholesterolCyclodextrinsmethyl-beta-cyclodextrinPotassium Channels, Inwardly Rectifying

Identifiers

PMID12496090
PMCPMC1302398
OpenAlexW1979709047

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.