Evidence map›Paper›PMID 25014655›Full record

ArticlePloS one2014

Essentially all excess fibroblast cholesterol moves from plasma membranes to intracellular compartments.

Yvonne Lange, Jin Ye, Theodore L Steck

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Nonvesicular cholesterol transport in physiology.The Journal of clinical investigation · 2025
    Review
  3. Article
  4. Towards a Unitary Hypothesis of Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Different Pathways of Cellular Cholesterol Efflux.Cell biochemistry and biophysics · 2022
    Review
  10. Lipid Signaling During Gamete Maturation.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Plasma membrane cholesterol trafficking in steroidogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Yvonne LangeDepartment of Pathology, Rush University Medical Center, Chicago, Illinois, United States of America.
Jin YeDepartment of Pathology, Rush University Medical Center, Chicago, Illinois, United States of America.
Theodore L SteckDepartment of Biochemistry and Molecular Biology, University of Chicago, Chicago, Illinois, United States of America.
Rush University Medical Center · USUniversity of Chicago · US

Funding

THE DYNAMICS OF CHOLESTEROL IN MEMBRANESR01HL028448 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI LANGE, YVONNE · 1985 to 2012
$2.9M
DISPOSITION AND MOVEMENT OF CHOLESTEROL IN CELLSR55HL028448 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI LANGE, YVONNE · 1992 to 1992
–
NHLBI NIH HHS HL28448NHLBI NIH HHS R01 HL028448
6 · The paper itself

Abstract

It has been shown that modestly increasing plasma membrane cholesterol beyond its physiological set point greatly increases the endoplasmic reticulum and mitochondrial pools, thereby eliciting manifold feedback responses that return cell cholesterol to its resting state. The question arises whether this homeostatic mechanism reflects the targeting of cell surface cholesterol to specific intracellular sites or its general equilibration among the organelles. We now show that human fibroblast cholesterol can be increased as much as two-fold from 2-hydroxypropyl-β-cyclodextrin without changing the size of the cell surface pool. Rather, essentially all of the added cholesterol disperses rapidly among cytoplasmic membranes, increasing their overall cholesterol content by as much as five-fold. We conclude that the level of plasma membrane cholesterol is normally at capacity and that even small increments above this physiological set point redistribute essentially entirely to intracellular membranes, perhaps down their chemical activity gradients.

Indexed as

2-Hydroxypropyl-beta-cyclodextrinbeta-CyclodextrinsBiological TransportCell MembraneCholesterolEndoplasmic ReticulumFibroblastsForeskinHomeostasisHumansKineticsMaleMitochondriaOxidation-ReductionPrimary Cell Culture2-Hydroxypropyl-beta-cyclodextrinbeta-CyclodextrinsCholesterol

Identifiers

PMID25014655
PMCPMC4094430
OpenAlexW1988838278

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.