Evidence map›Paper›PMID 27140210›Full record

ArticleCNS neuroscience & therapeutics2016

Morphological and Functional Attenuation of Degeneration of Peripheral Neurons by Mesenchymal Stem Cell-Conditioned Medium in Spinocerebellar Ataxia Type 1-Knock-in Mice.

Nana Suto, Tokue Mieda, Akira Iizuka, Kazuhiro Nakamura, Hirokazu Hirai

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Genetics, Mechanisms, and Therapeutic Progress in Polyglutamine Spinocerebellar Ataxias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    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

5 authors at 1 institution in 1 country.

Nana SutoDepartment of Neurophysiology & Neural Repair, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Tokue MiedaDepartment of Orthopedic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Akira IizukaDepartment of Neurophysiology & Neural Repair, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Kazuhiro NakamuraDepartment of Neurophysiology & Neural Repair, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Hirokazu HiraiDepartment of Neurophysiology & Neural Repair, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Gunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsSpinocerebellar ataxia type 1 (SCA1) is caused by the ataxin-1 protein (ATXN1) with an abnormally expanded polyglutamine tract and is characterized by progressive neurodegeneration. We previously showed that intrathecal injection of mesenchymal stem cells (MSCs) during the nonsymptomatic stage mitigates the degeneration of the peripheral nervous system (PNS) neurons in SCA1-knock-in (SCA1-KI) mice. We tested in this study whether the therapeutic effects of MSCs in SCA1-KI mice could be reproduced with MSC-releasing factor(s).

methodsTo test the effects of MSC-releasing factor(s), we used MSC-conditioned medium (MSC-CM). MSC-CM was intrathecally and/or intravenously injected into young SCA1-KI mice, and the therapeutic effects were assessed in the PNS at later ages using immunostaining, electrophysiology, and behavioral tests.

resultsMSC-CM attenuated the degeneration of axons and myelin of spinal motor neurons. Consequently, the injected SCA1-KI mice exhibited smaller reductions in nerve conduction velocity in spinal motor neurons and reduced motor incoordination than the untreated mice.

conclusionsThese results suggest that factors released from MSC mitigate the morphological and functional abnormalities in the PNS that are observed in SCA1-KI mice in a paracrine manner.

Indexed as

Age FactorsAnimalsAtaxin-1AxonsCells, CulturedCulture Media, ConditionedDisease Models, AnimalEvoked Potentials, MotorHumansMesenchymal Stem CellsMiceMice, Inbred C57BLMice, TransgenicMotor ActivityMotor NeuronsMyelin Basic ProteinAtaxin-1ATXN1 protein, humanCulture Media, ConditionedMyelin Basic ProteinTubulinAxonConditioned mediumMesenchymal stem cellMyelinSCA1Spinal motor neuron

Identifiers

PMID27140210
PMCPMC6492824
OpenAlexW2345677745

What OpenQuestion holds

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Registered trials

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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.