Evidence map›Paper›PMID 33096826›Full record

ArticleInternational journal of molecular sciences2020

Enhancing the Therapeutic Potential of

Sanghun Lee, Ok Joon Kim, Kee Ook Lee, Hyeju Jung, Seung-Hun Oh, Nam Keun Kim

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

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Angiogenesis after ischemic stroke.Acta pharmacologica Sinica · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Sanghun LeeDepartment of Neurology, CHA Bundang Medical Center, CHA University, Seongnam 13496, Korea.
Ok Joon KimDepartment of Neurology, CHA Bundang Medical Center, CHA University, Seongnam 13496, Korea.ORCID 0000-0002-7333-0647
Kee Ook LeeDepartment of Neurology, CHA Bundang Medical Center, CHA University, Seongnam 13496, Korea.
Hyeju JungDepartment of Neurology, CHA Bundang Medical Center, CHA University, Seongnam 13496, Korea.
Seung-Hun OhDepartment of Neurology, CHA Bundang Medical Center, CHA University, Seongnam 13496, Korea.
Nam Keun KimInstitute for Clinical Research, CHA Bundang Medical Center, CHA University, Seongnam 13488, Korea.ORCID 0000-0003-0541-3528
CHA University Bundang Medical Center · KR

Funding

Ministry of Health and Welfare HI16C1559
6 · The paper itself

Abstract

Although intravenous administration of mesenchymal stem cells (MSCs) is effective for experimental stroke, low engraftment and the limited functional capacity of transplanted cells are critical hurdles for clinical applications. C-C motif chemokine ligand 2 (CCL2) is associated with neurological repair after stroke and delivery of various cells into the brain via CCL2/CCR2 (CCL2 receptor) interaction. In this study, after CCL2-overexpressing human umbilical cord-derived MSCs (hUC-MSCs) were intravenously transplanted with mannitol in rats with middle cerebral arterial occlusion, we compared the differences between four different treatment groups: mannitol + CCL2-overexpressing hUC-MSCs (CCL2-MSC), mannitol + naïve hUC-MSCs (M-MSC), mannitol only, and control. At four-weeks post-transplantation, the CCL2-MSC group showed significantly better functional recovery and smaller stroke volume relative to the other groups. Additionally, we observed upregulated levels of CCR2 in acute ischemic brain and the increase of migrated stem cells into these areas in the CCL2-MSC group relative to the M-MSC. Moreover, the CCL2-MSC group displayed increased angiogenesis and endogenous neurogenesis, decreased neuro-inflammation but with increased healing-process inflammatory cells relative to other groups. These findings indicated that CCL2-overexpressing hUC-MSCs showed better functional recovery relative to naïve hUC-MSCs according to the increased migration of these cells into brain areas of higher CCR2 expression, thereby promoting subsequent endogenous brain repair.

Indexed as

AnimalsBrainBrain IschemiaChemokine CCL2Disease Models, AnimalHumansInfarction, Middle Cerebral ArteryMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationNeovascularization, PhysiologicNeurogenesisRats, Sprague-DawleyReceptors, CCR2StrokeUmbilical CordCCL2 protein, humanCcl2 protein, ratCcr2 protein, ratChemokine CCL2Receptors, CCR2angiogenesisCCL2CCR2mesenchymal stem cellneurogenesisstroke

Identifiers

PMID33096826
PMCPMC7588958
OpenAlexW3093595499

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.