Evidence map›Paper›PMID 29511131›Full record

ArticleStroke2018

Endothelial Progenitor Cell Secretome and Oligovascular Repair in a Mouse Model of Prolonged Cerebral Hypoperfusion.

Takakuni Maki, Anna Morancho, Pablo Martinez-San Segundo, Kazuhide Hayakawa, Hajime Takase, Anna C Liang, Marina Gabriel-Salazar, Esperanza Medina-Gutiérrez, Kazuo Washida, Joan Montaner and 4 more

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

Article in Stroke, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  8. Article
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  11. A brief overview of a mouse model of cerebral hypoperfusion by bilateral carotid artery stenosis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
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  13. Article
  14. Article
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  16. Article
  17. Dysregulation of mTOR Signaling after Brain Ischemia.International journal of molecular sciences · 2022
    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

14 authors at 1 institution in 1 country.

Takakuni MakiFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Anna MoranchoFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Pablo Martinez-San SegundoFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Kazuhide HayakawaFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Hajime TakaseFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Anna C LiangFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Marina Gabriel-SalazarFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Esperanza Medina-GutiérrezFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Kazuo WashidaFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Joan MontanerFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Josephine LokFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Eng H LoFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Ken AraiFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.).
Anna RosellFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown (T.M., K.H., H.T., A.C.L., K.W., J.L., E.H.L., K.A.); and Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Spain (A.M., P.M.-S.S., M.G.-S., E.M.-G., J.M., A.R.). anna.rosell@vhir.org karai@partners.org.
Universitat Autònoma de Barcelona · ES

Funding

Targeting ROCK for Neurogliovascular Plasticity & Remodeling After StrokeP01NS055104 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2007 to 2018
$13.3M
Oligo-Vascular Signaling in StrokeR01NS065089 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN · 2010 to 2019
$3.8M
Proteomic Profiling of Patent Foramen Ovale Related Neurovascular InjuryR01NS067139 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI NING, MINGMING · 2010 to 2023
$3.7M
Thrombolysis Profiles in tPA ResponseR01NS093415 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H., NING, MINGMING · 2015 to 2019
$1.9M
Glycoproteomics in Ischemic Stroke Related HyperglycemiaR21NS113065 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI NING, MINGMING · 2020 to 2020
$462k
NINDS NIH HHS P01 NS055104NINDS NIH HHS R01 NS065089NINDS NIH HHS R01 NS067139NINDS NIH HHS R01 NS093415NINDS NIH HHS R21 NS113065
6 · The paper itself

Abstract

background and purposeEndothelial progenitor cells (EPCs) have been extensively investigated as a therapeutic approach for repairing the vascular system in cerebrovascular diseases. Beyond vascular regeneration per se, EPCs may also release factors that affect the entire neurovascular unit. Here, we aim to study the effects of the EPC secretome on oligovascular remodeling in a mouse model of white matter injury after prolonged cerebral hypoperfusion.

methodsThe secretome of mouse EPCs was analyzed with a proteome array. In vitro, the effects of the EPC secretome and its factor angiogenin were assessed on primary oligodendrocyte precursor cells and mature human cerebral microvascular endothelial cells (hCMED/D3). In vivo, mice were subjected to permanent bilateral common carotid artery stenosis, then treated with EPC secretome at 24 hours and at 1 week, and cognitive outcome was evaluated with the Y maze test together with oligodendrocyte precursor cell proliferation/differentiation and vascular density in white matter at 4 weeks.

resultsMultiple growth factors, cytokines, and proteases were identified in the EPC secretome, including angiogenin. In vitro, the EPC secretome significantly enhanced endothelial and oligodendrocyte precursor cell proliferation and potentiated oligodendrocyte precursor cell maturation. Angiogenin was proved to be a key factor since pharmacological blockade of angiogenin signaling negated the positive effects of the EPC secretome. In vivo, treatment with the EPC secretome increased vascular density, myelin, and mature oligodendrocytes in white matter and rescued cognitive function in the mouse hypoperfusion model.

conclusionsFactors secreted by EPCs may ameliorate white matter damage in the brain by boosting oligovascular remodeling.

Indexed as

Angiogenesis Inducing AgentsAnimalsBrain IschemiaCarotid StenosisCell ProliferationCulture Media, ConditionedCytokinesDisease Models, AnimalEndothelial Progenitor CellsGlutathione S-Transferase piHumansIntercellular Signaling Peptides and ProteinsIn Vitro TechniquesMiceMyelin Basic ProteinOligodendrocyte Precursor CellsAngiogenesis Inducing AgentsangiogeninCulture Media, ConditionedCytokinesGlutathione S-Transferase piIntercellular Signaling Peptides and ProteinsMyelin Basic ProteinPecam1 protein, mousePeptide HydrolasesPlatelet Endothelial Cell Adhesion Molecule-1Receptor, Platelet-Derived Growth Factor alphaRibonuclease, Pancreaticangiogenincarotid stenosisendothelial progenitor cellrepairwhite matter

Identifiers

PMID29511131
PMCPMC5871569
OpenAlexW2790199840

What OpenQuestion holds

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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.