Evidence map›Paper›PMID 21040449›Full record

ArticleJournal of thrombosis and haemostasis : JTH2011

Phosphatidylserine as an anchor for plasminogen and its plasminogen receptor, histone H2B, to the macrophage surface.

R Das, E F Plow

Abstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2011. 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
0.8field-weighted citation impact, top 29% 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, 33 citations in OpenAlex.

  1. Regulation of histones in thromboinflammation.Frontiers in immunology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. From plasminogen to plasmin: role of plasminogen receptors in human cancer.International journal of molecular sciences · 2014
    Review
  11. Article
  12. New insights into the role of Plg-RKT in macrophage recruitment.International review of cell and molecular biology · 2014
    Review
  13. Plasminogen receptors: the first quarter century.Seminars in thrombosis and hemostasis · 2013
    Review
  14. Article
  15. Article
  16. Article
  17. So many plasminogen receptors: why?Journal of biomedicine & biotechnology · 2012
    Review
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

2 authors at 1 institution in 1 country.

R DasDepartment of Molecular Cardiology, Cleveland Clinic, Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Cleveland, OH 44195, USA.
E F Plow
Cleveland Clinic · US

Funding

THE CLASSICAL AND ALTERNATIVE PATHWAYS OF FIBRINOLYSISR01HL017964 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI PLOW, EDWARD FRANKLIN · 1985 to 2015
$5.6M
NHLBI NIH HHS HL17964NHLBI NIH HHS R01 HL017964
6 · The paper itself

Abstract

backgroundPlasminogen (Plg) binding to cell surface Plg receptors (Plg-Rs) on the surface of macrophages facilitates Plg activation and migration of these cells. Histone H2B (H2B) acts as a Plg-R and its cell surface expression is up-regulated when monocytes are differentiated to macrophages via a pathway dependent on L-type Ca(2+) channels and intracellular Ca(2+).

objectivesWe sought to investigate the mechanism by which H2B, a protein without a transmembrane domain, is retained on the macrophage surface.

methodsTHP-1 monocytoid cells were induced to differentiate with interferon gamma + Vitamin D3 or to undergo apoptosis by treatment with camptothecin. Flow cytometry and cell surface biotinylation followed by Western blotting were used to measure the interrelationship between Plg binding, cell surface expression of H2B and outer membrane exposure of phosphatidylserine (PS).

resultsH2B interacted directly with PS via an electrostatic interaction. Anti-PS or PS binding proteins, annexin V and protein S, diminished H2B interaction with PS on the surface of differentiated or apoptotic cells and these same reagents inhibited Plg binding to these cells. L-type Ca(2+) channels played a significant role in PS exposure, H2B surface expression and Plg binding induced either by differentiation or apoptosis.

conclusionsThese data suggest that H2B tethers to the surface of cells by interacting with PS on differentiated or apoptotic monocytoid cells. L-type Ca(2+) channels regulate PS exposure on the surface of these cells. The exposed PS interacts directly with H2B and hence provides sites for Plg to bind to.

Indexed as

Blotting, WesternFlow CytometryHistonesHumansMacrophagesPhosphatidylserinesPlasminogenProtein BindingHistonesPhosphatidylserinesPlasminogen

Identifiers

PMID21040449
PMCPMC3881192
OpenAlexW1582138350

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.