Beating affects the post-transcriptional regulation of [alpha]
-myosin mrna in cardiac cultures.
Goldspink, Paul H., Donald B. Thomason, and Brenda Russell.
Department of Physiology and Biophysics (M/C 901), University of
Illinois College of Medicine at Chicago, 901 S Wolcott Ave, Chicago,
IL 60612-7342, Department of Physiology and Biophysics (D.B.T),
College of Medicine, University of Tennessee, 894 Union Ave, Memphis,
TN, 38163
APStracts 3:0260H, 1996.
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 post-transcriptional
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 (10
[mu]mol/L) verapamil (a Ca2+channel blocker) or by (5 mmol/L) 2,3
butanedione monoxime (BDM, a cross-bridge inhibitor). Inhibition of
transcription with amanitin (0.5 [mu]mol/L) decreased [alpha]-MHC
mRNA in normally beating myocytes to a minimal baseline. However, the
[alpha]-MHC mRNA did not fall this low in amanitin-treated, non
-beating myocytes. Concurrently, the [alpha]-MHC mRNA shifted towards
a heavier polysome complex when beating was blocked. Together, these
data suggest that contractile arrest regulates [alpha]-MHC mRNA
abundance post-transcriptionally by stabilizing the message at the
elongation phase of translation. These post-transcriptional
regulatory steps are dependent upon beating itself and are
independent of calcium entry.
Received 15 February 1996; accepted in final form 7 June 1996.
APS Manuscript Number H159-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96