Evidence map›Paper›PMID 36535938›Full record

ArticleNature communications2022

Endothelial cells regulate astrocyte to neural progenitor cell trans-differentiation in a mouse model of stroke.

Wenlu Li, Emiri T Mandeville, Violeta Durán-Laforet, Norito Fukuda, Zhanyang Yu, Yi Zheng, Aaron Held, Ji-Hyun Park, Takafumi Nakano, Masayoshi Tanaka and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. PEBP1 inhibition as a therapeutic target for neurological recovery in ischemic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  12. Brain endothelial HIF-1Acta pharmaceutica Sinica. B · 2025
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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

21 authors at 5 institutions in 3 countries.

Wenlu LiNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. wli23@mgh.harvard.edu.ORCID 0000-0001-6507-392X
Emiri T MandevilleNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-7680-0923
Violeta Durán-LaforetNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Norito FukudaNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-1548-0516
Zhanyang YuNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Yi ZhengNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Aaron HeldDepartment of Neurology, Sean M. Healey & AMG Center for ALS, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Ji-Hyun ParkNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Takafumi NakanoNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Masayoshi TanakaNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Jingfei ShiNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Elga EspositoNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Wanting NiuTissue Engineering Laboratories, VA Boston Healthcare System, Boston, MA, USA.
Changhong XingNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Kazuhide HayakawaNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-1229-2413
Ignacio LizasoainUnidad de Investigación Neurovascular, Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre, Madrid, Spain.ORCID 0000-0002-6028-7379
Klaus van LeyenNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Xunming JiCerebrovascular Research Institute, XuanWu Hospital, Capital Medical University, Beijing, China.ORCID 0000-0003-0293-2744
Brian J WaingerDepartment of Neurology, Sean M. Healey & AMG Center for ALS, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-3664-7231
Maria A MoroNeurovascular Pathophysiology Group, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0003-1010-8237
Eng H LoNeuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. lo@helix.mgh.harvard.edu.ORCID 0000-0002-9327-2915
Harvard University · USUniversidad Complutense de Madrid · ESBrigham and Women's Hospital · USCapital Medical University · CNSpanish National Centre for Cardiovascular Research · ES

Funding

Defining the molecular connections between hyperexcitability and neurodegeneration in ALSF32NS114319 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI HELD, AARON HARRY · 2020 to 2022
$136k
NINDS NIH HHS F32 NS114319
6 · The paper itself

Abstract

The concept of the neurovascular unit emphasizes the importance of cell-cell signaling between neural, glial, and vascular compartments. In neurogenesis, for example, brain endothelial cells play a key role by supplying trophic support to neural progenitors. Here, we describe a surprising phenomenon where brain endothelial cells may release trans-differentiation signals that convert astrocytes into neural progenitor cells in male mice after stroke. After oxygen-glucose deprivation, brain endothelial cells release microvesicles containing pro-neural factor Ascl1 that enter into astrocytes to induce their trans-differentiation into neural progenitors. In mouse models of focal cerebral ischemia, Ascl1 is upregulated in endothelium prior to astrocytic conversion into neural progenitor cells. Injecting brain endothelial-derived microvesicles amplifies the process of astrocyte trans-differentiation. Endothelial-specific overexpression of Ascl1 increases the local conversion of astrocytes into neural progenitors and improves behavioral recovery. Our findings describe an unexpected vascular-regulated mechanism of neuroplasticity that may open up therapeutic opportunities for improving outcomes after stroke.

Indexed as

Neural Stem CellsStrokeAnimalsAstrocytesCells, CulturedCell TransdifferentiationEndothelial CellsMaleMice

Identifiers

PMID36535938
PMCPMC9763251
OpenAlexW4313339554

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.