Myonuclear apoptosis via cleaved caspase-3 upregulation is related to macrophage accumulation underlying immobilization-induced muscle fibrosis.


Journal

Muscle & nerve
ISSN: 1097-4598
Titre abrégé: Muscle Nerve
Pays: United States
ID NLM: 7803146

Informations de publication

Date de publication:
03 2022
Historique:
revised: 08 11 2021
received: 13 03 2021
accepted: 04 12 2021
pubmed: 11 12 2021
medline: 19 3 2022
entrez: 10 12 2021
Statut: ppublish

Résumé

Although macrophage accumulation plays a key role in the development of immobilization-induced muscle fibrosis, the underlying mechanisms remain unclear. Therefore, we focused on the alterations of myonuclear apoptosis via cleaved caspase-3, and investigated whether these changes may be related to macrophage accumulation. Eight-week-old Wistar rats were divided into immobilization and control groups, and the soleus muscles were selected for analysis. The mRNA and protein expression of collagen and the number of CD11b-positive cells were significantly higher in the immobilized rats than in the control rats at 1 and 2 weeks. TdT-mediated dUTP nick end-labeling (TUNEL)-positive myonuclei counts in 1- and 2-week control rats were 0.2 ± 0.1 and 0.2 ± 0.5, whereas they were 1.0 ± 0.6 and 1.1 ± 0.5 in 1- and 2-week immobilized rats. The cleaved caspase-3 protein expressions in 1- and 2-week control rats were 0.2 ± 0.1 and 0.2 ± 0.1, whereas they were 0.5 ± 0.1 and 0.4 ± 0.2 in 1- and 2-week immobilized rats. TUNEL-positive myonuclei counts and cleaved caspase-3 protein expression were significantly higher in immobilized rats than in control rats at 1 and 2 weeks. The numbers of myonuclei in 1- and 2-week control rats were 2.8 ± 0.1 and 2.6 ± 0.4, whereas they were 2.2 ± 0.4 and 2.2 ± 0.2 in 1- and 2-week immobilized rats. The numbers of myonuclei were significantly lower in immobilized than in control rats at both time-points. Myonuclear apoptosis via the upregulation of cleaved caspase-3 might induce macrophage accumulation. These alterations are related to immobilization-induced muscle fibrosis.

Identifiants

pubmed: 34890049
doi: 10.1002/mus.27473
doi:

Substances chimiques

Casp3 protein, rat EC 3.4.22.-
Caspase 3 EC 3.4.22.-

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

341-349

Informations de copyright

© 2021 Wiley Periodicals LLC.

Références

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Auteurs

Natsumi Tanaka (N)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Department of Physical Therapy, School of Rehabilitation Sciences, Seirei Christopher University, Shizuoka, Japan.

Yuichiro Honda (Y)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Institute of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.

Yasuhiro Kajiwara (Y)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Department of Rehabilitation, Nagasaki University Hospital, Nagasaki, Japan.

Hideki Kataoka (H)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Department of Rehabilitation, Nagasaki Memorial Hospital, Nagasaki, Japan.

Tomoki Origuchi (T)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Institute of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.

Junya Sakamoto (J)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Institute of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.

Minoru Okita (M)

Department of Physical Therapy Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Institute of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.

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