Evidence map›Paper›PMID 29066780›Full record

ArticleScientific reports2017

Survival Motor Neuron Protein is Released from Cells in Exosomes: A Potential Biomarker for Spinal Muscular Atrophy.

Leslie A Nash, Emily R McFall, Amanda M Perozzo, Maddison Turner, Kathy L Poulin, Yves De Repentigny, Joseph K Burns, Hugh J McMillan, Jodi Warman Chardon, Dylan Burger and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  9. Bioengineering extracellular vesicle cargo for optimal therapeutic efficiency.Molecular therapy. Methods & clinical development · 2024
    Review
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  12. Article
  13. Review
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  16. Exosomes as Actively Targeted Nanocarriers for Cancer Therapy.International journal of nanomedicine · 2020
    Review
  17. 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

12 authors at 2 institutions in 1 country.

Leslie A NashRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Emily R McFallRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Amanda M PerozzoRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Maddison TurnerKidney Research Centre, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Kathy L PoulinRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Yves De RepentignyRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Joseph K BurnsRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Hugh J McMillanUniversity of Ottawa Centre for Neuromuscular Disease, Ottawa, Ontario, Canada.
Jodi Warman ChardonUniversity of Ottawa Centre for Neuromuscular Disease, Ottawa, Ontario, Canada.
Dylan BurgerKidney Research Centre, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Rashmi KotharyRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.ORCID 0000-0002-9239-7310
Robin J ParksRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada. rparks@ohri.ca.
University of Ottawa · CAOttawa Hospital · CA

Funding

CIHR MOP-130279CIHR MOP-136898CIHR MOP-142316
6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is caused by homozygous mutation of the survival motor neuron 1 (SMN1) gene. Disease severity inversely correlates to the amount of SMN protein produced from the homologous SMN2 gene. We show that SMN protein is naturally released in exosomes from all cell types examined. Fibroblasts from patients or a mouse model of SMA released exosomes containing reduced levels of SMN protein relative to normal controls. Cells overexpressing SMN protein released exosomes with dramatically elevated levels of SMN protein. We observed enhanced quantities of exosomes in the medium from SMN-depleted cells, and in serum from a mouse model of SMA and a patient with Type 3 SMA, suggesting that SMN-depletion causes a deregulation of exosome release or uptake. The quantity of SMN protein contained in the serum-derived exosomes correlated with the genotype of the animal, with progressively less protein in carrier and affected animals compared to wildtype mice. SMN protein was easily detectable in exosomes isolated from human serum, with a reduction in the amount of SMN protein in exosomes from a patient with Type 3 SMA compared to a normal control. Our results suggest that exosome-derived SMN protein may serve as an effective biomarker for SMA.

Indexed as

AnimalsBiomarkersCell LineExosomesHumansMiceMuscular Atrophy, SpinalSMN Complex ProteinsBiomarkersSMN Complex Proteins

Identifiers

PMID29066780
PMCPMC5655039
OpenAlexW2766995496

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.