Evidence map›Paper›PMID 34144647›Full record

ArticleCell transplantation

Intravenous Administration of Human Amniotic Mesenchymal Stem Cells in the Subacute Phase of Cerebral Infarction in a Mouse Model Ameliorates Neurological Disturbance by Suppressing Blood Brain Barrier Disruption and Apoptosis via Immunomodulation.

Yasunori Yoshida, Toshinori Takagi, Yoji Kuramoto, Kotaro Tatebayashi, Manabu Shirakawa, Kenichi Yamahara, Nobutaka Doe, Shinichi Yoshimura

Open access · goldAbstract read
In one paragraph

Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Brain repair mechanisms after cell therapy for stroke.Brain : a journal of neurology · 2024
    Review
  8. Review
  9. An update on stem cell therapy for stroke patients: Where are we now?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Review
  10. Review
  11. Article
  12. Mesenchymal Stem Cells and Their Exocytotic Vesicles.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Stem Cell- and Cell-Based Therapies for Ischemic Stroke.Bioengineering (Basel, Switzerland) · 2022
    Review
  15. Article
  16. Review
  17. Treatment of ischemic stroke with modified mesenchymal stem cells.International journal of medical sciences · 2022
    Review
  18. Review
  19. Review
  20. Article
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

8 authors at 2 institutions in 1 country.

Yasunori YoshidaDepartment of Neurosurgery, 12818Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, Japan.
Toshinori TakagiDepartment of Neurosurgery, 12818Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, Japan.
Yoji KuramotoDepartment of Neurosurgery, 12818Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, Japan.ORCID 0000-0002-3652-6261
Kotaro TatebayashiDepartment of Neurosurgery, 12818Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, Japan.
Manabu ShirakawaDepartment of Neurosurgery, 12818Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, Japan.
Kenichi YamaharaLaboratory of Medical Innovation, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Nobutaka DoeLaboratory of Neurogenesis and CNS Repair, 12818, Nishinomiya, Hyogo, Japan.
Shinichi YoshimuraDepartment of Neurosurgery, 12818Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, Japan.ORCID 0000-0001-5633-9132
Hyogo Medical University · JPHyogo University of Health Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuro-inflammation plays a key role in the pathophysiology of brain infarction. Cell therapy offers a novel therapeutic option due to its effect on immunomodulatory effects. Amniotic stem cells, in particular, show promise owing to their low immunogenicity, tumorigenicity, and easy availability from amniotic membranes discarded following birth. We have successfully isolated and expanded human amniotic mesenchymal stem cells (hAMSCs). Herein, we evaluated the therapeutic effect of hAMSCs on neurological deficits after brain infarction as well as their immunomodulatory effects in a mouse model in order to understand their mechanisms of action. One day after permanent occlusion of the middle cerebral artery (MCAO), hAMSCs were intravenously administered. RT-qPCR for TNFα, iNOS, MMP2, and MMP9, immunofluorescence staining for iNOS and CD11b/c, and a TUNEL assay were performed 8 days following MCAO. An Evans Blue assay and behavioral tests were performed 2 days and several months following MCAO, respectively. The results suggest that the neurological deficits caused by cerebral infarction are improved in dose-dependent manner by the administration of hAMSCs. The mechanism appears to be through a reduction in disruption of the blood brain barrier and apoptosis in the peri-infarct region through the suppression of pro-inflammatory cytokines and the M2-to-M1 phenotype shift.

Indexed as

Administration, IntravenousAnimalsApoptosisBlood-Brain BarrierDisease Models, AnimalHumansImmunomodulationInfarction, Middle Cerebral ArteryMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceSignal Transductionamnioncell therapyhuman amniotic mesenchymal stem cellsischemic strokeMCAOmouse

Identifiers

PMID34144647
PMCPMC8216398
OpenAlexW3170448735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.