Effects of glucocorticoids on peptide chain initiation in heart and skeletal muscle.

D. E. Rannels, S. R. Rannels, J. B. Li, Anthony Pegg, H. E. Morgan, Leonard "Jim" Jefferson

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Treatment of rats for 5 days with cortisone acetate reduced synthesis of skeletal muscle protein by 56% compared to untreated controls, but had no effect on protein synthesis in heart. The reduction in synthesis in skeletal muscle was accounted for by both a loss of tissue RNA and development of a block in peptide-chain initiation. Activity of an eIF-2-like initiation factor decreased in psoas muscle of hormone-treated rats in proportion to the loss of RNA. Peptide-chain initiation, RNA content, and initiation factor activity were unaffected in heart muscle. In skeletal muscle of rats treated for 4 hr with dexamethasone, peptide-chain initiation was inhibited, whereas tissue RNA content and initiation factor activity were unchanged. These experiments suggested that total activity of eIF-2 did not always correlate with the rate of initiation, but that there did appear to be a relationship between initiation factor activity and tissue RNA content. Purification of eIF-2 from bovine heart muscle was undertaken in order to directly investigate the mechanism by which glucocorticoids modify eIF-2-activity and control peptide-chain initiation.

Original languageEnglish (US)
Pages (from-to)493-501
Number of pages9
JournalAdvances in myocardiology
Volume1
StatePublished - Jan 1 1980

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Glucocorticoids
Myocardium
Skeletal Muscle
Peptide Initiation Factors
RNA
Peptides
Prokaryotic Initiation Factor-2
Psoas Muscles
Muscle Proteins
Dexamethasone
Hormones
Proteins

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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Effects of glucocorticoids on peptide chain initiation in heart and skeletal muscle. / Rannels, D. E.; Rannels, S. R.; Li, J. B.; Pegg, Anthony; Morgan, H. E.; Jefferson, Leonard "Jim".

In: Advances in myocardiology, Vol. 1, 01.01.1980, p. 493-501.

Research output: Contribution to journalArticle

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