Evidence map›Paper›PMID 26965847›Full record

ArticleStroke2016

Astrocyte-Derived Pentraxin 3 Supports Blood-Brain Barrier Integrity Under Acute Phase of Stroke.

Akihiro Shindo, Takakuni Maki, Emiri T Mandeville, Anna C Liang, Naohiro Egawa, Kanako Itoh, Naoki Itoh, Mia Borlongan, Julie C Holder, Tsu Tshen Chuang and 5 more

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

Article in Stroke, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

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18 more citing papers are in PubMed but not listed here.

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

15 authors at 1 institution in 1 country.

Akihiro ShindoFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Takakuni MakiFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Emiri T MandevilleFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Anna C LiangFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Naohiro EgawaFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Kanako ItohFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Naoki ItohFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Mia BorlonganFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Julie C HolderFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Tsu Tshen ChuangFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
John D McNeishFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Hidekazu TomimotoFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Josephine LokFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Eng H LoFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
Ken AraiFrom the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.). karai@partners.org.
GlaxoSmithKline (United Kingdom) · GB

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
NINDS NIH HHS P01 NS055104NINDS NIH HHS P01-NS55104NINDS NIH HHS R01 NS065089NINDS NIH HHS R01-NS065089
6 · The paper itself

Abstract

background and purposePentraxin 3 (PTX3) is released on inflammatory responses in many organs. However, roles of PTX3 in brain are still mostly unknown. Here we asked whether and how PTX3 contributes to blood-brain barrier dysfunction during the acute phase of ischemic stroke.

methodsIn vivo, spontaneously hypertensive rats were subjected to focal cerebral ischemia by transient middle cerebral artery occlusion. At day 3, brains were analyzed to evaluate the cellular origin of PTX3 expression. Correlations with blood-brain barrier breakdown were assessed by IgG staining. In vitro, rat primary astrocytes and rat brain endothelial RBE.4 cells were cultured to study the role of astrocyte-derived PTX3 on vascular endothelial growth factor-mediated endothelial permeability.

resultsDuring the acute phase of stroke, reactive astrocytes in the peri-infarct area expressed PTX3. There was negative correlation between gradients of IgG leakage and PTX3-positive astrocytes. Cell culture experiments showed that astrocyte-conditioned media increased levels of tight junction proteins and reduced endothelial permeability under normal conditions. Removing PTX3 from astrocyte-conditioned media by immunoprecipitation increased endothelial permeability. PTX3 strongly bound vascular endothelial growth factor in vitro and was able to decrease vascular endothelial growth factor-induced endothelial permeability.

conclusionsAstrocytes in peri-infarct areas upregulate PTX3, which may support blood-brain barrier integrity by regulating vascular endothelial growth factor-related mechanisms. This response in astrocytes may comprise a compensatory mechanism for maintaining blood-brain barrier function after ischemic stroke.

Indexed as

AnimalsAstrocytesBlood-Brain BarrierBrainCell DeathC-Reactive ProteinCulture Media, ConditionedEndothelial CellsEndothelium, VascularInfarction, Middle Cerebral ArteryMalePentraxinsRatsRats, Inbred SHRSerum Amyloid P-ComponentStrokeC-Reactive ProteinCulture Media, ConditionedPentraxinsSerum Amyloid P-ComponentVascular Endothelial Growth Factor Aastrocyteblood–brain barriercell–cell interactionendotheliumstroke

Identifiers

PMID26965847
PMCPMC4811738
OpenAlexW2295673115

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.