Evidence map›Paper›PMID 19667108›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2009

Membrane cholesterol is a biomechanical regulator of neutrophil adhesion.

Hana Oh, Emile R Mohler, Aiwei Tian, Tobias Baumgart, Scott L Diamond

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. The role of neutrophils in the pathogenesis of abdominal aortic aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Article
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  15. Review
  16. Cholesterol and the Safety Factor for Neuromuscular Transmission.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Potential role of Lu/BCAM in HIV-related atherosclerosis.African journal of laboratory medicine · 2019
    Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Hana OhDepartment of Chemical and Biomolecular Engineering, Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, USA.
Emile R Mohler
Aiwei Tian
Tobias Baumgart
Scott L Diamond
University of the Sciences · US

Funding

MECHANISMS OF NONVIRAL CARDIOVASCULAR GENE TRANSFERR01HL066565 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DIAMOND, SCOTT L · 2001 to 2013
$3.6M
Reaction and Transport Dynamics in Human BloodR01HL056621 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DIAMOND, SCOTT L · 1996 to 2009
$1.8M
NHLBI NIH HHS HL 56621NHLBI NIH HHS HL 66565NHLBI NIH HHS R01 HL056621NHLBI NIH HHS R01 HL066565
6 · The paper itself

Abstract

objectiveThe purpose of this study was to evaluate the role of membrane cholesterol on human neutrophil and HL-60 biomechanics, capture, rolling, and arrest to P-selectin- or IL-1-activated endothelium. METHODS AND

resultsMethyl-beta-cyclodextrin (MbetaCD) removed up to 73% and 45% of membrane cholesterol from HL-60 cells and neutrophils, whereas MbetaCD/cholesterol complexes resulted in maximum enrichment of 65% and 40%, respectively, above control levels. Cells were perfused at a venous wall shear rate of 100 s(-1) over adherent P-selectin-coated 1-microm diameter beads, uncoated 10-mum diameter beads, P-selectin-coated surfaces, or activated endothelium. Elevated cholesterol enhanced capture efficiency to 1-microm beads and increased membrane tether growth rate by 1.5- to 2-fold, whereas cholesterol depletion greatly reduced tether formation. Elevated cholesterol levels increased tether lifetime by 17% in neutrophils and adhesion lifetime by 63% in HL-60 cells. Deformation of cholesterol-enriched neutrophils increased the contact time with 10-mum beads by 32% and the contact area by 7-fold. On both P-selectin surfaces and endothelial-cell monolayers, cholesterol-enriched neutrophils rolled more slowly, more stably, and were more likely to firmly arrest. Cholesterol depletion resulted in opposite effects.

conclusionsIncreasing membrane cholesterol enhanced membrane tether formation and whole cell deformability, contributing to slower, more stable rolling on P-selectin and increased firm arrest on activated endothelium.

Indexed as

Cell AdhesionLeukocyte Rollingbeta-CyclodextrinsBiomechanical PhenomenaCell MembraneCholesterolDose-Response Relationship, DrugEndothelial CellsHL-60 CellsHumansInterleukin-1Membrane GlycoproteinsNeutrophilsP-SelectinTime Factorsbeta-CyclodextrinsCholesterolInterleukin-1Membrane Glycoproteinsmethyl-beta-cyclodextrinP-SelectinP-selectin ligand protein

Identifiers

PMID19667108
PMCPMC2762395
OpenAlexW2153101062

What OpenQuestion holds

Textmetadata
LicenceTDM
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.