Dental pulp stem cells can improve muscle dysfunction in animal models of Duchenne muscular dystrophy.


Journal

Stem cell research & therapy
ISSN: 1757-6512
Titre abrégé: Stem Cell Res Ther
Pays: England
ID NLM: 101527581

Informations de publication

Date de publication:
25 01 2021
Historique:
received: 13 10 2020
accepted: 13 12 2020
entrez: 26 1 2021
pubmed: 27 1 2021
medline: 6 7 2021
Statut: epublish

Résumé

Duchenne muscular dystrophy (DMD) is an inherited progressive disorder that causes skeletal and cardiac muscle deterioration with chronic inflammation. Dental pulp stem cells (DPSCs) are attractive candidates for cell-based strategies for DMD because of their immunosuppressive properties. Therefore, we hypothesized that systemic treatment with DPSCs might show therapeutic benefits as an anti-inflammatory therapy. To investigate the potential benefits of DPSC transplantation for DMD, we examined disease progression in a DMD animal model, mdx mice, by comparing them with different systemic treatment conditions. The DPSC-treated model, a canine X-linked muscular dystrophy model in Japan (CXMD We demonstrated a therapeutic strategy for long-term functional recovery in DMD using repeated DPSC administration. DPSC-treated mdx mice and CXMD We developed a novel strategy for the safe and effective transplantation of DPSCs for DMD recovery, which included repeated systemic injection to regulate inflammation at a young age. This is the first report on the efficacy of a systemic DPSC treatment, from which we can propose that DPSCs may play an important role in delaying the DMD disease phenotype.

Sections du résumé

BACKGROUND
Duchenne muscular dystrophy (DMD) is an inherited progressive disorder that causes skeletal and cardiac muscle deterioration with chronic inflammation. Dental pulp stem cells (DPSCs) are attractive candidates for cell-based strategies for DMD because of their immunosuppressive properties. Therefore, we hypothesized that systemic treatment with DPSCs might show therapeutic benefits as an anti-inflammatory therapy.
METHODS
To investigate the potential benefits of DPSC transplantation for DMD, we examined disease progression in a DMD animal model, mdx mice, by comparing them with different systemic treatment conditions. The DPSC-treated model, a canine X-linked muscular dystrophy model in Japan (CXMD
RESULTS
We demonstrated a therapeutic strategy for long-term functional recovery in DMD using repeated DPSC administration. DPSC-treated mdx mice and CXMD
CONCLUSIONS
We developed a novel strategy for the safe and effective transplantation of DPSCs for DMD recovery, which included repeated systemic injection to regulate inflammation at a young age. This is the first report on the efficacy of a systemic DPSC treatment, from which we can propose that DPSCs may play an important role in delaying the DMD disease phenotype.

Identifiants

pubmed: 33494794
doi: 10.1186/s13287-020-02099-3
pii: 10.1186/s13287-020-02099-3
pmc: PMC7831244
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

78

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Auteurs

Yuko Nitahara-Kasahara (Y)

Department of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan. y-kasahara@nms.ac.jp.
Division of Cell and Gene Therapy, Nippon Medical School, Bunkyo-city, Tokyo, Japan. y-kasahara@nms.ac.jp.
Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. y-kasahara@nms.ac.jp.

Mutsuki Kuraoka (M)

Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Laboratory of Experimental Animal Science, Nippon Veterinary and Life Science University, Musashino, Tokyo, Japan.

Posadas Herrera Guillermo (PH)

Department of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan.
Division of Molecular and Medical Genetics, Center for Gene and Cell Therapy, Institute of Medical Science, The University of Tokyo, Minato-city, Tokyo, Japan.

Hiromi Hayashita-Kinoh (H)

Division of Cell and Gene Therapy, Nippon Medical School, Bunkyo-city, Tokyo, Japan.
Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Division of Molecular and Medical Genetics, Center for Gene and Cell Therapy, Institute of Medical Science, The University of Tokyo, Minato-city, Tokyo, Japan.

Yasunobu Maruoka (Y)

Department of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan.

Aki Nakamura-Takahasi (A)

Department of Pharmacology, Tokyo Dental College, Tokyo, Japan.

Koichi Kimura (K)

Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Department of General Medicine, The Institute of Medical Science, The University of Tokyo, Minato-city, Tokyo, Japan.

Shin'ichi Takeda (S)

Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.

Takashi Okada (T)

Division of Cell and Gene Therapy, Nippon Medical School, Bunkyo-city, Tokyo, Japan. t-okada@ims.u-tokyo.ac.jp.
Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. t-okada@ims.u-tokyo.ac.jp.
Division of Molecular and Medical Genetics, Center for Gene and Cell Therapy, Institute of Medical Science, The University of Tokyo, Minato-city, Tokyo, Japan. t-okada@ims.u-tokyo.ac.jp.

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