Evidence map›Paper›PMID 32341395›Full record

ArticleScientific reports2020

Heterogenetic parabiosis between healthy and dystrophic mice improve the histopathology in muscular dystrophy.

Aiping Lu, Ping Guo, Liang Wang, Chieh Tseng, Matthieu Huard, Chris Allen, Ruth McCarrick-Walmsley, Kaitlyn E Whitney, Johnny Huard

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

9 authors.

Aiping LuSteadman Philippon Research Institute, Vail, CO, 81657, USA. alu@sprivail.org.
Ping GuoSteadman Philippon Research Institute, Vail, CO, 81657, USA.
Liang WangDepartment of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, GD, 510080, China.
Chieh TsengDepartment of Orthopaedic Surgery, The University of Texas Health Science Center at Houston, Houston, TX, 77054, USA.
Matthieu HuardSteadman Philippon Research Institute, Vail, CO, 81657, USA.
Chris AllenDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO, 80523-1681, USA.
Ruth McCarrick-WalmsleySteadman Philippon Research Institute, Vail, CO, 81657, USA.
Kaitlyn E WhitneySteadman Philippon Research Institute, Vail, CO, 81657, USA.
Johnny HuardSteadman Philippon Research Institute, Vail, CO, 81657, USA. jhuard@sprivail.org.

Funding

Bone Abnormalities & Healing Defect in Muscular DystrophyR01AR065445 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HUARD, JOHNNY · 2014 to 2018
$1.7M
NIAMS NIH HHS R01 AR065445
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a progressive muscle disease, characterized by mutations in the X-linked dystrophin, that has several therapeutic options but no curative treatment. Transplantation of muscle progenitor cells for treatment of DMD has been widely investigated; however, its application is hindered by limited cell survival due to the harmful dystrophic microenvironment. An alternative approach to utilize progenitor cells and circulatory factors and to improve the dystrophic muscle pathology and microenvironment is through parabiotic pairing, where mice are surgically sutured to create a joint circulatory system. Parabiotic mice were generated by surgically joining wild type (WT) mice expressing green fluorescent protein (GFP) with mdx mice. These mice developed a common circulation (approximately 50% green cells in the blood of mdx mice) 2-weeks after parabiotic pairing. We observed significantly improved dystrophic muscle pathology, including decreased inflammation, necrotic fibers and fibrosis in heterogenetic parabionts. Importantly, the GFP + cells isolated from the mdx mice (paired with GFP mice) underwent myogenic differentiation in vitro and expressed markers of mesenchymal stem cells and macrophages, which may potentially be involved in the improvement of dystrophic muscle pathology. These observations suggest that changing the dystrophic microenvironment can be a new approach to treat DMD.

Indexed as

ParabiosisAnimalsAntigens, DifferentiationMesenchymal Stem CellsMiceMice, Inbred mdxMice, TransgenicMuscle, SkeletalMuscular Dystrophy, DuchenneAntigens, Differentiation

Identifiers

PMID32341395
PMCPMC7184587

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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.