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Purification and transplantation of myogenic progenitor cell derived exosomes to improve cardiac function in duchenne muscular dystrophic mice

*Corresponding author for this work
  • Shanghai Jiao Tong University
    ,
  • Medical College of Georgia
    ,
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

Duchene Muscular Dystrophy (DMD) is an X-linked recessive genetic disease caused by a lack of functional dystrophin protein. The disease cannot be cured, and as the disease progresses, the patient develops symptoms of dilated cardiomyopathy, arrhythmia, and congestive heart failure. The DMD MDX mutant mice do not express dystrophin, and are commonly used as a mouse model of DMD. In our recent study, we observed that intramyocardial injection of wide type (WT)-myogenic progenitor cells-derived exosomes (MPC-Exo) transiently restored the expression of dystrophin in the myocardium of DMD MDX mutant mice, which was associated with a transient improvement in cardiac function suggesting that WT-MPC-Exo may provide an option to relieve the cardiac symptoms of DMD. This article describes the technique of MPC-Exo purification and transplantation into hearts of DMD MDX mutant mice.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Article number

e59320

Journal (Volume, Issue Number)

Journal of Visualized Experiments (Volume 2019, Issue 146)

Publication milestones

  • Published - 04/2019

Publication status

Published - 04/2019

ISSN

1940-087X

Publication IDs

  • Scopus: 85065392555
  • PubMed: 31033952

Publication metrics

Metrics

SciVal
FWCI
0.59
SciVal
Author count
6
SciVal
citations
4
SciVal
Paper percentile
72
Fractional count
2
Fractional count
0.33
Fractional count
4
Fractional count
0.67
Fractional count
2
Fractional count
1
Scopus
citations

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Citation count
10
Captures
22

Funding Details

Tang were partially supported by the American Heart Association: GRNT31430008, NIH-AR070029, NIH-HL086555, NIH-HL134354.