Evidence map›Paper›PMID 28445478›Full record

ArticlePloS one2017

Delayed histochemical alterations within the neurovascular unit due to transient focal cerebral ischemia and experimental treatment with neurotrophic factors.

Dominik Michalski, Roman Pitsch, Deepu R Pillai, Bianca Mages, Susanne Aleithe, Jens Grosche, Henrik Martens, Felix Schlachetzki, Wolfgang Härtig

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. 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

9 authors at 3 institutions in 1 country.

Dominik MichalskiDepartment of Neurology, University of Leipzig, Liebigstr. 20, Leipzig, Germany.
Roman PitschPaul Flechsig Institute for Brain Research, University of Leipzig, Liebigstr. 19, Leipzig, Germany.
Deepu R PillaiDepartment of Neurology, University of Regensburg and Clinic for Neurological Rehabilitation II, Universitätsstr. 84, Regensburg, Germany.
Bianca MagesDepartment of Neurology, University of Leipzig, Liebigstr. 20, Leipzig, Germany.
Susanne AleitheDepartment of Neurology, University of Leipzig, Liebigstr. 20, Leipzig, Germany.
Jens GroscheEffigos GmbH, Am Deutschen Platz 4, Leipzig, Germany.
Henrik MartensSynaptic Systems, Göttingen, Germany.
Felix SchlachetzkiDepartment of Neurology, University of Regensburg and Clinic for Neurological Rehabilitation II, Universitätsstr. 84, Regensburg, Germany.
Wolfgang HärtigPaul Flechsig Institute for Brain Research, University of Leipzig, Liebigstr. 19, Leipzig, Germany.
Leipzig University · DEForschungszentrum Jülich · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current stroke therapy is focused on recanalizing strategies, but neuroprotective co-treatments are still lacking. Modern concepts of the ischemia-affected neurovascular unit (NVU) and surrounding penumbra emphasize the complexity during the transition from initial damaging to regenerative processes. While early treatment with neurotrophic factors was shown to result in lesion size reduction and blood-brain barrier (BBB) stabilization, cellular consequences from these treatments are poorly understood. This study explored delayed cellular responses not only to ischemic stroke, but also to an early treatment with neurotrophic factors. Rats underwent 60 minutes of focal cerebral ischemia. Fluorescence labeling was applied to sections from brains perfused 7 days after ischemia. Analyses focused on NVU constituents including the vasculature, astrocytes and microglia in the ischemic striatum, the border zone and the contralateral hemisphere. In addition to histochemical signs of BBB breakdown, a strong up-regulation of collagen IV and microglia activation occurred within the ischemic core with simultaneous degradation of astrocytes and their endfeet. Activated astroglia were mainly depicted at the border zone in terms of a glial scar formation. Early treatment with pigment epithelium-derived factor (PEDF) resulted in an attenuation of the usually up-regulated collagen IV-immunoreactivity. However, glial activation was not influenced by treatment with PEDF or the epidermal growth factor (EGF). In conclusion, these data on ischemia-induced cellular reactions within the NVU might help to develop treatments addressing the transition from injury towards regeneration. Thereby, the integrity of the vasculature in close relation to neighboring structures like astrocytes appears as a promising target.

Indexed as

AnimalsAquaporin 4AstrocytesBlood-Brain BarrierBrainCollagen Type IVDisease Models, AnimalEpidermal Growth FactorEye ProteinsGlial Fibrillary Acidic ProteinIschemic Attack, TransientMagnetic Resonance ImagingMaleMicrogliaMicroscopy, FluorescenceNerve Growth FactorsAquaporin 4Collagen Type IVEpidermal Growth FactorEye ProteinsGfap protein, ratGlial Fibrillary Acidic ProteinNerve Growth FactorsPigment Epithelium-Derived FactorSerpinsVascular Endothelial Growth Factor A

Identifiers

PMID28445478
PMCPMC5405989
OpenAlexW2607933433

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.