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Muscle Nerve. 2013 May;47(5):711-21. doi: 10.1002/mus.23642. Epub 2013 Feb 9.

Lack of caspase-3 attenuates immobilization-induced muscle atrophy and loss of tension generation along with mitigation of apoptosis and inflammation.

Author information

1
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Shriners Hospitals for Children, Room 206, 5l Blossom Street, Boston, Massachusetts 02114, USA.

Abstract

INTRODUCTION:

Immobilization by casting induces disuse muscle atrophy (DMA).

METHODS:

Using wild type (WT) and caspase-3 knockout (KO) mice, we evaluated the effect of caspase-3 on muscle mass, apoptosis, and inflammation during DMA.

RESULTS:

Caspase-3 deficiency significantly attenuated muscle mass decrease [gastrocnemius: 28 ± 1% in KO vs. 41 ± 3% in WT; soleus: 47 ± 2% in KO vs. 56 ± 2% in WT; (P < 0.05)] and gastrocnemius twitch tension decrease (23 ± 4% in KO vs. 36 ± 3% in WT, P < 0.05) at day 14 in immobilized vs. contralateral hindlimb. Lack of caspase-3 decreased immobilization-induced increased apoptotic myonuclei (3.2-fold) and macrophage infiltration (2.2-fold) in soleus muscle and attenuated increased monocyte chemoattractant protein-1 mRNA expression (2-fold in KO vs. 18-fold in WT) in gastrocnemius.

CONCLUSIONS:

Caspase-3 plays a key role in DMA and associated decreased tension, presumably by acting on the apoptosis and inflammation pathways.

PMID:
23401051
PMCID:
PMC3634903
DOI:
10.1002/mus.23642
[Indexed for MEDLINE]
Free PMC Article

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