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increases ubiquitin-conjugating activity in skeletal muscle by up-regulating UbcH2/E220k
Department of Medicine, Baylor College of Medicine, Houston, Texas, USA;
* Renal Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA;
AstraZeneca Pharmaceuticals, Alderley Park, Cheshire, England, SK10 4TG; and
Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA
1Correspondence: Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Suite 520B, Houston, TX 77030, USA. E-mail: reid{at}bcm.tmc.edu
In some inflammatory diseases, TNF-
is thought to stimulate muscle catabolism via an NF-
B-dependent process that increases ubiquitin conjugation to muscle proteins. The transcriptional mechanism of this response has not been determined. Here we studied the potential role of UbcH2, a ubiquitin carrier protein and homologue of murine E220k. We find that UbcH2 is constitutively expressed by human skeletal and cardiac muscles, murine limb muscle, and cultured myotubes. TNF- stimulates UbcH2 expression in mouse limb muscles in vivo and in cultured myotubes. The UbcH2 promoter region contains a functional NF-B binding site; NF-B binding to this sequence is increased by TNF- stimulation. A dominant negative inhibitor of NF-B activation blocks both UbcH2 up-regulation and the increase in ubiquitin-conjugating activity stimulated by TNF-. In extracts from TNF--treated myotubes, ubiquitin-conjugating activity is limited by UbcH2 availability; activity is inhibited by an antiserum to UbcH2 or a dominant negative mutant of UbcH2 and is enhanced by wild-type UbcH2. Thus, UbcH2 up-regulation is a novel response to TNF-/NF-B signaling in skeletal muscle that appears to be essential for the increased ubiquitin conjugation induced by this cytokine.—Li, Y.-P., Lecker, S. H., Chen, Y., Waddell, I. D., Goldberg, A. L., Reid, M. B. TNF- increases ubiquitin-conjugating activity in skeletal muscle by up-regulating UbcH2/E220k.
Key Words: cachexia • catabolism • atrophy • cytokines • nuclear factor B
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