Evidence map›Paper›PMID 29282083›Full record

ArticleJournal of neuroinflammation2017

Tissue transglutaminase in astrocytes is enhanced by inflammatory mediators and is involved in the formation of fibronectin fibril-like structures.

Nathaly Espitia Pinzón, John J P Brevé, John G J M Bol, Benjamin Drukarch, Wia Baron, Anne-Marie van Dam

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. The Role of Transglutaminase 2 in Cancer: An Update.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. 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 2 institutions in 1 country.

Nathaly Espitia PinzónDepartment Anatomy and Neurosciences, VU University Medical Center, Amsterdam Neuroscience, De Boelelaan 1108, 1081, HZ, Amsterdam, The Netherlands.
John J P BrevéDepartment Anatomy and Neurosciences, VU University Medical Center, Amsterdam Neuroscience, De Boelelaan 1108, 1081, HZ, Amsterdam, The Netherlands.
John G J M BolDepartment Anatomy and Neurosciences, VU University Medical Center, Amsterdam Neuroscience, De Boelelaan 1108, 1081, HZ, Amsterdam, The Netherlands.
Benjamin DrukarchDepartment Anatomy and Neurosciences, VU University Medical Center, Amsterdam Neuroscience, De Boelelaan 1108, 1081, HZ, Amsterdam, The Netherlands.
Wia BaronDepartment of Cell Biology, University Medical Center Groningen, Groningen, The Netherlands.
Anne-Marie van DamDepartment Anatomy and Neurosciences, VU University Medical Center, Amsterdam Neuroscience, De Boelelaan 1108, 1081, HZ, Amsterdam, The Netherlands. amw.vandam@vumc.nl.
Amsterdam Neuroscience · NLUniversity Medical Center Groningen · NL

Funding

Stichting MS Research 09-693MS
6 · The paper itself

Abstract

backgroundDuring multiple sclerosis (MS) lesion formation, inflammatory mediators are produced by microglial cells and invading leukocytes. Subsequently, hypertrophic astrocytes fill the lesion and produce extracellular matrix (ECM) proteins that together form the astroglial scar. This is beneficial because it seals off the site of central nervous system (CNS) damage. However, astroglial scarring also forms an obstacle that inhibits remyelination of brain lesions. This is possibly an important cause for incomplete remyelination of the CNS in early stage MS patients and for failure of remyelination when the disease progresses. Tissue transglutaminase (TG2), a Ca

methodsThe effect of different inflammatory mediators on TG2 and fibronectin, an ECM protein, protein levels was examined in primary rat microglia and astrocytes by western blotting. Also, TG2 activity was analyzed in primary rat astrocytes by a TG activity assay. To determine the role of TG2 in the deposition and cross-linking of fibronectin, a TG2 inhibitor and TG2 knockdown astrocytes were used.

resultsOur data show that under inflammatory conditions in vitro, TG2 production is enhanced in astrocytes and microglia. We observed that in particular, astrocytes produce fibronectin that can be cross-linked and aggregated by exogenous TG2. Moreover, inflammatory stimulus-induced endogenously produced TG2 is involved in the appearance of morphological fibril-like fibronectin deposits but does not lead to cross-linked fibronectin aggregates.

conclusionsOur in vitro observations suggest that during MS lesion formation, when inflammatory mediators are produced, astrocyte-derived TG2 may contribute to ECM rearrangement, and subsequent astroglial scarring.

Indexed as

AnimalsAstrocytesCerebral CortexExtracellular MatrixFibronectinsGTP-Binding ProteinsInflammation MediatorsMicrogliaProtein Glutamine gamma Glutamyltransferase 2RatsRats, WistarTransglutaminasesFibronectinsGTP-Binding ProteinsInflammation MediatorsProtein Glutamine gamma Glutamyltransferase 2Tgm2 protein, ratTransglutaminasesAstrocytesAstroglial scarringExtracellular matrixFibronectinNeuroinflammationTissue transglutaminase

Identifiers

PMID29282083
PMCPMC5745633
OpenAlexW2776196354

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.