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Cited by 731

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions

Open access
Du, Jie, Wang, Xiaonan, Miereles, Christiane, Bailey, James L., Debigare, Richard, Zheng, Bin, Price, S. Russ, Mitch, William E.·2004·Journal of Clinical Investigation
DOI 10.1172/jci18330
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Abstract

With trauma, sepsis, cancer, or uremia, animals or patients experience accelerated degradation of muscle protein in the ATP-ubiquitin-proteasome (Ub-P'some) system. The initial step in myofibrillar proteolysis is unknown because this proteolytic system does not break down actomyosin complexes or myofibrils, even though it degrades monomeric actin or myosin. Since cytokines or insulin resistance are common in catabolic states and will activate caspases, we examined whether caspase-3 would break down actomyosin. We found that recombinant caspase-3 cleaves actomyosin, producing a characteristic, approximately 14-kDa actin fragment and other proteins that are degraded by the Ub-P'some. In fact, limited actomyosin cleavage by caspase-3 yields a 125% increase in protein degradation by the Ub-P'some system. Serum deprivation of L6 muscle cells stimulates actin cleavage and proteolysis; insulin blocks these responses by a mechanism requiring PI3K. Cleaved actin fragments are present in muscles of rats with muscle atrophy from diabetes or chronic uremia. Accumulation of actin fragments and the rate of proteolysis in muscle stimulated by diabetes are suppressed by a caspase-3 inhibitor. Thus, in catabolic conditions, an initial step resulting in loss of muscle protein is activation of caspase-3, yielding proteins that are degraded by the Ub-P'some system. Therapeutic strategies could be designed to prevent these events.

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Metadata

Authors
Du, J., Wang, X., Miereles, C., Bailey, J. L., Debigare, R., Zheng, B., Price, S. R., & Mitch, W. E.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2004-01-01
Volume
113
Issue
1
Pages
115-123
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci18330
OpenAlex
W2154584639
Cited by
731
References
1
FWCI
14.00
Type
journal article
Language
en
Open access
bronze

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