Evidence map›Paper›PMID 33406093›Full record

ArticlePloS one2021

Neuroprotection mediated by ST266 requires full complement of proteins secreted by amnion-derived multipotent progenitor cells.

Keirnan Willett, Reas S Khan, Kimberly Dine, Howard Wessel, Ziv Z Kirshner, Jodie L Sauer, Ashley Ellis, Larry R Brown, Kenneth S Shindler

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Nanoparticles Enhance Solubility and Neuroprotective Effects of Resveratrol in Demyelinating Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  5. Article
  6. Article
  7. 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

9 authors at 1 institution in 1 country.

Keirnan WillettDepartment of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Reas S KhanDepartment of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Kimberly DineDepartment of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0001-5569-7261
Howard WesselNoveome Biotherapeutics, Inc., Pittsburgh, Pennsylvania, United States of America.
Ziv Z KirshnerNoveome Biotherapeutics, Inc., Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-6570-4602
Jodie L SauerNoveome Biotherapeutics, Inc., Pittsburgh, Pennsylvania, United States of America.
Ashley EllisNoveome Biotherapeutics, Inc., Pittsburgh, Pennsylvania, United States of America.
Larry R BrownNoveome Biotherapeutics, Inc., Pittsburgh, Pennsylvania, United States of America.
Kenneth S ShindlerDepartment of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0003-2417-258X
Penn Presbyterian Medical Center · US

Funding

Mechanism of SIRT1 Activator Mediated Neuroprotection of Retinal Ganglion CellsR01EY019014 · NEI · UNIVERSITY OF PENNSYLVANIA · PI SHINDLER, KENNETH S · 2010 to 2020
$3.7M
NEI NIH HHS R01 EY019014
6 · The paper itself

Abstract

ST266 is the biological secretome of cultured Amnion-derived Multipotent Progenitor cells containing multiple growth factors and cytokines. While intranasally-administered ST266 improves the phenotype in experimental optic neuritis, specific ST266 components mediating these effects are not known. We compared the effects of ST266 with and without removal of large molecular weight proteins both in vitro and in the multiple sclerosis model experimental autoimmune encephalomyelitis (EAE) in C57BL/6J mice. Mice were treated daily with intranasal vehicle, ST266 or lower molecular weight fraction of ST266. Retinal ganglion cells were counted in isolated retinas, and optic nerves were assessed for inflammation and demyelination. ST266 treatment significantly improved retinal ganglion cell survival and reduced optic nerve demyelination in EAE mice. The lower molecular weight ST266 fraction significantly improved optic nerve demyelination, but only showed a trend towards improved retinal ganglion cell survival. ST266 fractions below 50kDa increased Schwann cell proliferation in vitro, but were less effective than non-fractionated ST266. Demyelination attenuation was partially associated with the lower molecular weight ST266 fraction, but removal of higher molecular weight biomolecules from ST266 diminishes its neuroprotective effects, suggesting at least some high molecular weight proteins play a role in ST266-mediated neuroprotection.

Indexed as

NeuroprotectionAmnionAnimalsCell ProliferationDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalFemaleMiceMice, Inbred C57BLMolecular WeightMultipotent Stem CellsMyelin-Oligodendrocyte GlycoproteinOptic NerveOptic NeuritisPeptidesRetinal Ganglion CellsMyelin-Oligodendrocyte GlycoproteinPeptides

Identifiers

PMID33406093
PMCPMC7787369
OpenAlexW3119723141

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.