Evidence map›Paper›PMID 30153459›Full record

ArticleBrain research2018

Hyperfibrinogenemia-mediated astrocyte activation.

Vincent D Clark, Ailey Layson, Mariam Charkviani, Nino Muradashvili, David Lominadze

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

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  12. Fibrinogen Interaction with Astrocyte ICAM-1 and PrPInternational journal of molecular sciences · 2021
    Article
  13. Fibrinogen and/or Fibrin as a Cause of Neuroinflammation.Online journal of neurology and brain disorders · 2021
    Article
  14. Review
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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

5 authors at 1 institution in 2 countries.

Vincent D ClarkDepartment of Physiology, University of Louisville, School of Medicine, Louisville, KY, USA.
Ailey LaysonDepartment of Physiology, University of Louisville, School of Medicine, Louisville, KY, USA.
Mariam CharkvianiDepartment of Physiology, University of Louisville, School of Medicine, Louisville, KY, USA.
Nino MuradashviliDepartment of Physiology, University of Louisville, School of Medicine, Louisville, KY, USA; Department of Basic Medicine, Caucasus International University, Tbilisi, Georgia.
David LominadzeDepartment of Physiology, University of Louisville, School of Medicine, Louisville, KY, USA; Kentucky Spinal Cord Research Center, University of Louisville, School of Medicine, Louisville, KY, USA. Electronic address: david.lominadze@louisville.edu.
University of Louisville · US

Funding

Mechanisms of Homocysteine-Induced Fibrinogen-Amyloid Plaque FormationR01NS084823 · NINDS · UNIVERSITY OF LOUISVILLE · PI LOMINADZE, DAVID, TYAGI, SURESH C. · 2013 to 2017
$2.7M
NINDS NIH HHS R01 NS084823
6 · The paper itself

Abstract

Fibrinogen (Fg)-containing plaques are associated with memory loss during various inflammatory neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis, stroke, and traumatic brain injury. However, mechanisms of its action in neurovascular unit are not clear. As Fg is a high molecular weight blood protein and cannot translocate far from the vessel after extravasation, we hypothesized that it may interact with astrocytes first causing their activation. Cultured mouse cortical astrocytes were treated with Fg in the presence or absence of function-blocking anti-mouse intercellular adhesion molecule 1 (ICAM-1) antibody, or with medium alone (control). Expressions of ICAM-1 and tyrosine receptor kinase B (TrkB) as markers of astrocyte activation, and phosphorylation of TrkB (pTrkB) were assessed. Fg dose-dependently increased activation of astrocytes defined by their shape change, retraction of processes, and enhanced expressions of ICAM-1 and TrkB, and increased pTrkB. Blocking of ICAM-1 function ameliorated these Fg effects. Data suggest that Fg interacts with astrocytes causing overexpression of ICAM-1 and TrkB, and TrkB phosphorylation, and thus, astrocyte activation. Since TrkB is known to be involved in neurodegeneration, interaction of Fg with astrocytes and the resultant activation of TrkB can be a possible mechanism involved in memory reduction, which were observed in previous studies and were associated with formation of complexes of Fg deposited in extravascular space with proteins such as Amyloid beta or prion, the proteins involved in development of dementia.

Indexed as

AnimalsAstrocytesCells, CulturedCerebral CortexFibrinogenHumansIntercellular Adhesion Molecule-1Membrane GlycoproteinsMicePhosphorylationProtein-Tyrosine KinasesReceptor, trkBFibrinogenIntercellular Adhesion Molecule-1Membrane GlycoproteinsNtrk2 protein, mouseProtein-Tyrosine KinasesReceptor, trkBAstrocyteFibrinogenICAM-1TrkB

Identifiers

PMID30153459
PMCPMC6195850
OpenAlexW2888757621

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.