Evidence map›Paper›PMID 28290152›Full record

ArticleMolecular neurobiology2018

Vascular Endothelial Growth Factor Isoform-B Stimulates Neurovascular Repair After Ischemic Stroke by Promoting the Function of Pericytes via Vascular Endothelial Growth Factor Receptor-1.

Noëmie Jean LeBlanc, Revathy Guruswamy, Ayman ElAli

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

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  8. Research progress and challenges of stem cell therapy for ischemic stroke.Frontiers in cell and developmental biology · 2024
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  18. Neurovascular Unit: A critical role in ischemic stroke.CNS neuroscience & therapeutics · 2021
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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

3 authors at 1 institution in 1 country.

Noëmie Jean LeBlancNeuroscience Axis, CHU de Québec Research Center (CHUL) and Department of Psychiatry and Neuroscience, Faculty of Medicine, Laval University, 2705 Laurier Boulevard, Quebec City, QC, G1V 4G2, Canada.
Revathy GuruswamyNeuroscience Axis, CHU de Québec Research Center (CHUL) and Department of Psychiatry and Neuroscience, Faculty of Medicine, Laval University, 2705 Laurier Boulevard, Quebec City, QC, G1V 4G2, Canada.
Ayman ElAliNeuroscience Axis, CHU de Québec Research Center (CHUL) and Department of Psychiatry and Neuroscience, Faculty of Medicine, Laval University, 2705 Laurier Boulevard, Quebec City, QC, G1V 4G2, Canada. ayman.el-ali@crchudequebec.ulaval.ca.
Université Laval · CA

Funding

Fondation CHU de Québec 2331
6 · The paper itself

Abstract

Ischemic stroke triggers endogenous angiogenic mechanisms, which correlates with longer survival in patients. As such, promoting angiogenesis appears to be a promising approach. Experimental studies investigated mostly the potent angiogenic factor vascular endothelial growth factor isoform-A (VEGF-A). However, VEGF-A increases the risk of destabilizing the brain microvasculature, thus hindering the translation of its usage in clinics. An attractive alternative VEGF isoform-B (VEGF-B) was recently reported to act as a survival factor rather than a potent angiogenic factor. In this study, we investigated the therapeutic potential of VEGF-B in ischemic stroke using different in vivo and in vitro approaches. We showed that the delayed intranasal administration of VEGF-B reduced neuronal damage and inflammation. Unexpectedly, VEGF-B stimulated the formation of stable brain microvasculature within the injured region by promoting the interaction between endothelial cells and pericytes. Our data indicate that the effects of VEGF-B were mediated via its specific receptor VEGF receptor-1 (VEGFR-1) that is predominately expressed in brain pericytes. Importantly, VEGF-B promoted the survival of pericytes, and not brain endothelial cells, by inducing expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and the main protein involved in energy homeostasis AMP-activated protein kinase α (AMPKα). Moreover, we showed that VEGF-B stimulated the pericytic release of factors stimulating a "reparative angiogenesis" that does not compromise microvasculature stability. Our study unraveled hitherto unknown role of VEGF-B/VEGFR-1 signaling in regulating the function of pericytes. Furthermore, our findings suggest that brain microvasculature stabilization via VEGF-B constitutes a safe therapeutic approach for ischemic stroke.

Indexed as

Administration, IntranasalAnimalsBrain IschemiaDisease Models, AnimalEndothelial CellsEndothelium, VascularMaleMiceNeovascularization, PathologicPericytesSignal TransductionStrokeVascular Endothelial Growth Factor BVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor BVascular Endothelial Growth Factor Receptor-1AngiogenesisEndothelial cellsPericytesRepairStrokeVEGF-BVEGFR-1

Identifiers

PMID28290152
OpenAlexW2595100469

What OpenQuestion holds

Textmetadata
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.