Evidence map›Paper›PMID 25593138›Full record

ArticleStroke2015

Deficiency of brain ATP-binding cassette transporter A-1 exacerbates blood-brain barrier and white matter damage after stroke.

Xu Cui, Michael Chopp, Alex Zacharek, Joanna M Karasinska, Yisheng Cui, Ruizhuo Ning, Yi Zhang, Yun Wang, Jieli Chen

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

Article in Stroke, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

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  11. PTPN2 in the Immunity and Tumor Immunotherapy: A Concise Review.International journal of molecular sciences · 2022
    Review
  12. Diabetes complications and extracellular vesicle therapy.Reviews in endocrine & metabolic disorders · 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

9 authors at 2 institutions in 1 country.

Xu CuiFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.). tcui@neuro.hfh.edu jieli@neuro.hfh.edu.
Michael ChoppFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Alex ZacharekFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Joanna M KarasinskaFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Yisheng CuiFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Ruizhuo NingFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Yi ZhangFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Yun WangFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
Jieli ChenFrom the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.). tcui@neuro.hfh.edu jieli@neuro.hfh.edu.
Oakland University · USNational Institute on Drug Abuse · US

Funding

Neurorestorative therapy of stroke with HUCBC in type two diabetic miceR01NS083078 · NINDS · HENRY FORD HEALTH SYSTEM · PI CHEN, JIELI · 2014 to 2018
$1.6M
ABCA1 regulates white matter remodeling and oligodendrogenesis after strokeR01NS092917 · NINDS · HENRY FORD HEALTH SYSTEM · PI CUI, XU · 2015 to 2019
$1.6M
MSCs Induce Brain Plasticity via tPAR01AG037506 · NIA · HENRY FORD HEALTH SYSTEM · PI CHOPP, MICHAEL · 2011 to 2015
$1.5M
Neurorestorative therapy of stroke with agents that increase HDLR01AG031811 · NIA · HENRY FORD HEALTH SYSTEM · PI CHEN, JIELI · 2009 to 2013
$1.4M
Neurorestorative therapy of stroke with HUCBC in T2DM ratsR41NS080329 · NINDS · SANERON CCEL THERAPEUTICS, INC. · PI CHEN, JIELI · 2013 to 2014
$423k
NIA NIH HHS R01 AG031811NIA NIH HHS R01 AG037506NINDS NIH HHS 1R41NS080329-01A1NINDS NIH HHS R01 NS083078NINDS NIH HHS R01 NS092917NINDS NIH HHS R41 NS080329
6 · The paper itself

Abstract

background and purposeThe ATP-binding cassette transporter A-1 (ABCA1) gene is a key target of the transcription factors liver X receptors. Liver X receptor activation has anti-inflammatory and neuroprotective effects in animal ischemic stroke models. Here, we tested the hypothesis that brain ABCA1 reduces blood-brain barrier (BBB) and white matter (WM) impairment in the ischemic brain after stroke.

methodsAdult brain-specific ABCA1-deficient (ABCA1(-B/-B)) and floxed-control (ABCA1(fl/fl)) mice were subjected to permanent distal middle cerebral artery occlusion and were euthanized 7 days after distal middle cerebral artery occlusion. Functional outcome, infarct volume, BBB leakage, and WM damage were analyzed.

resultsCompared with ABCA1(fl/fl) mice, ABCA1(-B/-B) mice showed marginally (P=0.052) increased lesion volume but significantly increased BBB leakage and WM damage in the ischemic brain and more severe neurological deficits. Brain ABCA1-deficient mice exhibited increased the level of matrix metalloproteinase-9 and reduced the level of insulin-like growth factor 1 in the ischemic brain. BBB leakage was inversely correlated (r=-0.073; P<0.05) with aquaporin-4 expression. Reduction of insulin-like growth factor 1 and aquaporin-4, but upregulation of matrix metalloproteinase-9 expression were also found in the primary astrocyte cultures derived from ABCA1(-B/-B) mice. Cultured primary cortical neurons derived from C57BL/6 wild-type mice with ABCA1(-B/-B) astrocyte-conditioned medium exhibited decreased neurite outgrowth compared with culture with ABCA1(fl/fl) astrocyte-conditioned medium. ABCA1(-B/-B) primary cortical neurons show significantly decreased neurite outgrowth, which was attenuated by insulin-like growth factor 1 treatment.

conclusionsWe demonstrate that brain ABCA1 deficiency increases BBB leakage, WM/axonal damage, and functional deficits after stroke. Concomitant reduction of insulin-like growth factor 1 and upregulation of matrix metalloproteinase-9 may contribute to brain ABCA1 deficiency-induced BBB and WM/axonal damage in the ischemic brain.

Indexed as

AnimalsAstrocytesATP Binding Cassette Transporter 1Blood-Brain BarrierBrain InjuriesCells, CulturedDisease Models, AnimalImmunohistochemistryInfarction, Middle Cerebral ArteryInsulin-Like Growth Factor IMaleMatrix Metalloproteinase 9MiceMice, KnockoutMice, TransgenicStrokeAbca1 protein, mouseATP Binding Cassette Transporter 1insulin-like growth factor-1, mouseInsulin-Like Growth Factor IMatrix Metalloproteinase 9Mmp9 protein, mouseaquaporin 4ATP binding cassette transporter A-1blood–brain barrierinsulin-like growth factor binding protein 1strokewhite matter

Identifiers

PMID25593138
PMCPMC4342295
OpenAlexW2084847443

What OpenQuestion holds

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LicenceTDM
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.