Alcohol increases c-myc mRNA and protein in skeletal and cardiac muscle

Metabolism. 2002 Oct;51(10):1285-90. doi: 10.1053/meta.2002.34709.

Abstract

The pathogenic mechanisms responsible for alcohol-induced muscle disease are unknown, although it is possible that increased proto-oncogene expression may be the causative process. Therefore, we investigated the responses of skeletal muscle c-myc protein and mRNA to a standard acute ethanol dosage regimen (75 mmol/kg/body weight [BW]) for 2.5 to 24 hours. Comparative studies were made on the heart. Acute ethanol administration in vivo led to an increase in c-myc proto-oncogene mRNA in rat skeletal and cardiac muscle. The changes in c-myc mRNA were mirrored by increases in the c-myc protein as demonstrated by immunohistochemistry. The changes in the c-myc protein were localized to the myonuclei, with no corresponding changes seen in the interstitial cell nuclei. This is the first report of altered proto-oncogene expression in muscle in response to ethanol. Increased c-myc mRNA and protein may reflect adaptive changes, a stress response, or another uncharacterized cellular adaptation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoradiography
  • Blotting, Northern
  • Central Nervous System Depressants / pharmacology*
  • Ethanol / pharmacology*
  • Genes, myc / genetics*
  • Immunohistochemistry
  • Male
  • Muscle Proteins / biosynthesis*
  • Muscle, Skeletal / metabolism*
  • Myocardium / metabolism*
  • Proto-Oncogene Proteins c-myc / biosynthesis*
  • Proto-Oncogene Proteins c-myc / genetics
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis*
  • RNA, Messenger / genetics
  • Rats
  • Starvation / metabolism
  • Stimulation, Chemical
  • Up-Regulation / drug effects

Substances

  • Central Nervous System Depressants
  • Muscle Proteins
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • Ethanol