Evidence map›Paper›PMID 18166221›Full record

ArticleThrombosis research2008

Regulated complement deposition on the surface of human endothelial cells: effect of tobacco smoke and shear stress.

Wei Yin, Berhane Ghebrehiwet, Babette Weksler, Ellinor I B Peerschke

Open access · greenAbstract read
In one paragraph

Article in Thrombosis research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  9. Review
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  12. P-selectin drives complement attack on endothelium during intravascular hemolysis in TLR-4/heme-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Observational
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  15. Article
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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

4 authors at 2 institutions in 1 country.

Wei YinDepartment of Pathology and Laboratory of Medicine, Weill Medical College of Cornell University, New York, New York, USA.
Berhane Ghebrehiwet
Babette Weksler
Ellinor I B Peerschke
Cornell University · USStony Brook University · US

Funding

gC1q-R/p33: structure function and role on inflammation.R01AI060866 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHEBREHIWET, BERHANE · 2006 to 2009
$1.2M
gClqR/p33 in S. Aureus Endovascular PathogenesisR01HL067211 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI PEERSCHKE, ELLINOR I · 2002 to 2005
$1.2M
gC1q-R/P33: Structure-function and role in inflammationR56AI060866 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHEBREHIWET, BERHANE · 2012 to 2012
$377k
NHLBI NIH HHS HL67211NHLBI NIH HHS R01 HL067211NIAID NIH HHS AI060866NIAID NIH HHS R01 AI060866NIAID NIH HHS R56 AI060866
6 · The paper itself

Abstract

Cigarette smoke and hemodynamic stress both contribute to vascular inflammation and associated atherosclerosis. We recently demonstrated direct activation of complement components C4 and C3 on human endothelial cells (EC). The present study was designed to explore complement activation on bone marrow microvascular endothelial cells (BMEC) and human umbilical vein endothelial cells (HUVEC) in response to endothelial cell injury by tobacco smoke extract, shear stress, or other known inflammatory and atherogenic mediators, lipopolysaccharide (LPS) and INF-gamma. Following treatment, confluent EC monolayers were exposed to plasma (60 min, 37 degrees C), and cell surface deposition of stable complement derivatives C4d, iC3b and SC5b-9 was measured in situ using an ELISA approach. Consistent with previous results, moderate levels of C4d, iC3b and SC5b-9 deposition were observed on native EC monolayers exposed to human plasma. Tobacco smoke and shear stress enhanced EC C4d deposition. In contrast, LPS and INF-gamma failed to affect EC mediated complement activation, despite evidence of EC activation illustrated by ICAM-1 expression. The combination of tobacco smoke and shear stress nearly doubled EC C4d expression. No increases in iC3b or SC5b-9 were noted, suggesting inhibition of classical and alternative pathway C3 convertase assembly or activity. Indeed, concomitantly increased surface expression of complement regulatory proteins CD35 (CR1) and CD55 was observed following EC exposure to tobacco smoke and shear stress. These results suggest that a balance between complement activation and regulation exists at the EC surface, and may impact vascular injury leading to thrombosis, arteriosclerosis, and atherogenesis.

Indexed as

AnimalsBone Marrow CellsCD55 AntigensComplement ActivationComplement System ProteinsEndothelial CellsHemodynamicsHumansInterferon-gammaLipopolysaccharidesMiceMicrocirculationReceptors, Complement 3bSmokingStress, MechanicalUmbilical VeinsCD55 AntigensComplement System ProteinsInterferon-gammaLipopolysaccharidesReceptors, Complement 3b

Identifiers

PMID18166221
PMCPMC2633021
OpenAlexW2076514240

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.