Evidence map›Paper›PMID 31888056›Full record

ArticleCells2019

CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age.

Simone Lieschke, Bozena Zechmeister, Matteo Haupt, Xuan Zheng, Fengyan Jin, Katharina Hein, Martin S Weber, Dirk M Hermann, Mathias Bähr, Ertugrul Kilic and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. 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
0.9field-weighted citation impact, top 24% 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, 15 citations in OpenAlex.

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  8. The association ofFrontiers in neurology · 2022
    Article
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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

11 authors at 4 institutions in 3 countries.

Simone LieschkeDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Bozena ZechmeisterDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Matteo HauptDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Xuan ZhengDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Fengyan JinDepartment of Hematology, Cancer Center, The First Hospital of Jilin University, 2660 Jiefang Rd., Changchun 130021, China.
Katharina HeinDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Martin S WeberDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Dirk M HermannDepartment of Neurology, University of Duisburg-Essen, Hufelandstr. 55, 45147 Essen, Germany.
Mathias BährDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
Ertugrul KilicDepartment of Physiology, Istanbul Medipol University, Ekinciler Caddesi No. 19, Beykoz/İstanbul TR 34810, Turkey.ORCID 0000-0001-6494-8923
Thorsten R DoeppnerDepartment of Neurology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany.
University of Göttingen · DEIstanbul Medipol University · TRJilin University · CNUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCL11 has recently been shown to differentially affect cell survival under various pathological conditions including stroke. Indeed, CCL11 promotes neuroregeneration in neonatal stroke mice. The impact of CCL11 on the adult ischemic brain, however, remains elusive. We therefore studied the effect of ectopic CCL11 on both adolescent (six-week) and adult (six-month) C57BL6 mice exposed to stroke. Intraperitoneal application of CCL11 significantly aggravated acute brain injury in adult mice but not in adolescent mice. Likewise, post-stroke neurological recovery after four weeks was significantly impaired in adult mice whilst CCL11 was present. On the contrary, CCL11 stimulated gliogenesis and neurogenesis in adolescent mice. Flow cytometry analysis of blood and brain samples revealed a modification of inflammation by CCL11 at subacute stages of the disease. In adolescent mice, CCL11 enhances microglial cell, B and T lymphocyte migration towards the brain, whereas only the number of B lymphocytes is increased in the adult brain. Finally, the CCL11 inhibitor SB297006 significantly reversed the aforementioned effects. Our study, for the first time, demonstrates CCL11 to be a key player in mediating secondary cell injury under stroke conditions. Interfering with this pathway, as shown for SB297006, might thus be an interesting approach for future stroke treatment paradigms.

Indexed as

Disease SusceptibilityAge FactorsAnimalsApoptosisAutophagyBiomarkersBrain InfarctionBrain InjuriesBrain IschemiaChemokine CCL11Disease Models, AnimalDisease ProgressionImmunohistochemistryImmunophenotypingMaleMiceBiomarkersCcl11 protein, mouseChemokine CCL11CCL11cerebral ischemiaeotaxin-1inflammationneuroprotectionneuroregenerationstroke

Identifiers

PMID31888056
PMCPMC7017112
OpenAlexW2998108559

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.