Evidence map›Paper›PMID 28836238›Full record

ArticleTranslational stroke research2018

Protective Effects of Autologous Bone Marrow Mononuclear Cells After Administering t-PA in an Embolic Stroke Model.

Bing Yang, Weilang Li, Nikunj Satani, Duyen M Nghiem, XiaoPei Xi, Jaroslaw Aronowski, Sean I Savitz

Abstract read
PubMed Publisher
In one paragraph

Article in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Brain repair mechanisms after cell therapy for stroke.Brain : a journal of neurology · 2024
    Review
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  9. Recent Advances in Cell-Based Therapies for Ischemic Stroke.International journal of molecular sciences · 2020
    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

7 authors at 3 institutions in 2 countries.

Bing YangInstitute for Stroke and Cerebrovascular Disease and Department of Neurology, McGovern Medical School, University of Texas Health Science Center (UTHealth) at Houston, Houston, 77030, TX, USA. Bing.Yang@uth.tmc.edu.ORCID 0000-0001-6860-583X
Weilang LiDepartment of Neurology, Tongde Hospital of Zhejiang Province, Hangzhou, China.
Nikunj SataniInstitute for Stroke and Cerebrovascular Disease and Department of Neurology, McGovern Medical School, University of Texas Health Science Center (UTHealth) at Houston, Houston, 77030, TX, USA.
Duyen M NghiemInstitute for Stroke and Cerebrovascular Disease and Department of Neurology, McGovern Medical School, University of Texas Health Science Center (UTHealth) at Houston, Houston, 77030, TX, USA.
XiaoPei XiInstitute for Stroke and Cerebrovascular Disease and Department of Neurology, McGovern Medical School, University of Texas Health Science Center (UTHealth) at Houston, Houston, 77030, TX, USA.
Jaroslaw AronowskiInstitute for Stroke and Cerebrovascular Disease and Department of Neurology, McGovern Medical School, University of Texas Health Science Center (UTHealth) at Houston, Houston, 77030, TX, USA.
Sean I SavitzInstitute for Stroke and Cerebrovascular Disease and Department of Neurology, McGovern Medical School, University of Texas Health Science Center (UTHealth) at Houston, Houston, 77030, TX, USA.
The University of Texas Health Science Center at Houston · USThe University of Texas Health Science Center · USTongde Hospital of Zhejiang Province · CN

Funding

NIH HHS R01NS071127 and R21NS064316
6 · The paper itself

Abstract

Tissue plasminogen activator (t-PA) is the only FDA-approved drug for acute ischemic stroke but poses risk for hemorrhagic transformation (HT). Cell therapy has been investigated as a potential therapy to improve recovery after stroke by the modulation of inflammatory responses and the improvement of blood-brain barrier (BBB) integrity, both of which are associated with HT after t-PA. In our present study, we studied the effect of autologous bone marrow mononuclear cells (MNCs) in an embolic stroke model. We administered MNCs in a rat embolic stroke 2 h after administering t-PA. We observed that even though autologous MNCs did not alter the incidence of HT, they decreased the severity of HT and reduced BBB permeability. One possible mechanism could be through the inhibition of MMP3 released by astrocytes via JAK/STAT pathway as shown by our in vitro cell interaction studies.

Indexed as

AnimalsAnimals, NewbornAstrocytesBlood-Brain BarrierBone Marrow CellsCells, CulturedCerebral InfarctionCerebrovascular CirculationCoculture TechniquesCytokinesDisease Models, AnimalEmbryo, MammalianFemaleFibrinolytic AgentsGene Expression RegulationGlial Fibrillary Acidic ProteinCytokinesFibrinolytic AgentsGlial Fibrillary Acidic ProteinGlucoseMatrix Metalloproteinase 3Tissue Plasminogen ActivatorBlood-brain barrier integrityCellular therapyEmbolic strokeHemorrhagic transformationReperfusion injury

Identifiers

PMID28836238
OpenAlexW2748787550

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.