Evidence map›Paper›PMID 24612416›Full record

ArticleJournal of thrombosis and haemostasis : JTH2014

Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain.

K Hultman, M Cortes-Canteli, A Bounoutas, A T Richards, S Strickland, E H Norris

Open access · greenAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2014. 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
2.7field-weighted citation impact, top 10% 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, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Using antifibrinolytics to tackle neuroinflammation.Neural regeneration research · 2020
    Review
  7. A critical role for plasminogen in inflammation.The Journal of experimental medicine · 2020
    Review
  8. Anticoagulants for Treatment of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Blood-derived plasminogen drives brain inflammation and plaque deposition in a mouse model of Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. Blood will out: vascular contributions to Alzheimer's disease.The Journal of clinical investigation · 2018
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Plasminogen Deficiency Delays the Onset and Protects from Demyelination and Paralysis in Autoimmune Neuroinflammatory Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

6 authors at 1 institution in 1 country.

K HultmanThe Rockefeller University, New York, NY, USA.
M Cortes-Canteli
A Bounoutas
A T Richards
S Strickland
E H Norris
Rockefeller University · US

Funding

Role of the tPA/plasmin System in Alzheimers DiseaseR01NS050537 · NINDS · ROCKEFELLER UNIVERSITY · PI STRICKLAND, SIDNEY · 2004 to 2015
$5.7M
NINDS NIH HHS NS50537NINDS NIH HHS R01 NS050537
6 · The paper itself

Abstract

backgroundExcess fibrin in blood vessels is cleared by plasmin, the key proteolytic enzyme in fibrinolysis. Neurological disorders and head trauma can result in the disruption of the neurovasculature and the entry of fibrin and other blood components into the brain, which may contribute to further neurological dysfunction.

objectivesWhile chronic fibrin deposition is often implicated in neurological disorders, the pathological contributions attributable specifically to fibrin have been difficult to ascertain. An animal model that spontaneously acquires fibrin deposits could allow researchers to better understand the impact of fibrin in neurological disorders.

methodsBrains of plasminogen (plg)- and tissue plasminogen activator (tPA)-deficient mice were examined and characterized with regard to fibrin accumulation, vascular and neuronal health, and inflammation. Furthermore, the inflammatory response following intrahippocampal lipopolysaccharide (LPS) injection was compared between plg(-/-) and wild type (WT) mice. RESULTS AND

conclusionsBoth plg(-/-) and tPA(-/-) mice exhibited brain parenchymal fibrin deposits that appear to result from reduced neurovascular integrity. Markers of neuronal health and inflammation were not significantly affected by proximity to the vascular lesions. A compromised neuroinflammatory response was also observed in plg(-/-) compared to WT mice following intrahippocampal LPS injection. These results demonstrate that fibrin does not affect neuronal health in the absence of inflammation and suggest that plasmin may be necessary for a normal neuroinflammatory response in the mouse CNS.

Indexed as

AnimalsAstrocytesBrainFemaleFibrinFibrinolysinFibrinolysisHippocampusInflammationLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsPlasminogenFibrinFibrinolysinLipopolysaccharidesPlasminogenTissue Plasminogen Activatorfibrininflammationplasmintissue plasminogen activatorvasculature

Identifiers

PMID24612416
PMCPMC4120644
OpenAlexW2147177389

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.