Beating affects the posttranscriptional regulation of alpha-myosin mRNA in cardiac cultures. Am J Physiol 1996 Dec;271(6 Pt 2):H2584-90
Date
12/01/1996Pubmed ID
8997319DOI
10.1152/ajpheart.1996.271.6.H2584Scopus ID
2-s2.0-0030475772 (requires institutional sign-in at Scopus site) 25 CitationsAbstract
Contractile arrest of cardiac myocytes results in increased abundance of alpha-myosin heavy chain (MHC) mRNA but decreased alpha-MHC protein content. Our aim is to determine the posttranscriptional mechanisms regulating alpha-MHC mRNA-protein uncoupling in cultured neonatal rat hearts during altered contractile activity. Spontaneously contracting myocytes were arrested by the use of verapamil (10 mumol/l; a Ca(2+)-channel blocker) or by 2,3-butanedione monoxime (5 mmol/l; a cross-bridge inhibitor). Inhibition of transcription with amanitin (0.5 mumol/l) decreased the alpha-MHC mRNA in normally beating myocytes to a minimal baseline. However, the alpha-MHC mRNA did not fall this low in amanitin-treated nonbeating myocytes. Concurrently, the alpha-MHC mRNA shifted toward a heavier polysome complex when beating was blocked. Together, these data suggest that contractile arrest regulates alpha-MHC mRNA abundance posttranscriptionally by stabilizing the message at the elongation phase of translation. These posttranscriptional regulatory steps are dependent on beating itself and are independent of Ca2+ entry.
Author List
Goldspink PH, Thomason DB, Russell BMESH terms used to index this publication - Major topics in bold
AnimalsCells, Cultured
Diacetyl
Drug Stability
Myocardial Contraction
Myocardium
Myosin Heavy Chains
Myosins
Polyribosomes
Protein Processing, Post-Translational
RNA, Messenger
Rats
Rats, Sprague-Dawley
Tissue Distribution
