Small amounts of alpha-myosin heavy chain isoform expression significantly increase power output of rat cardiac myocyte fragments.
Myocardial performance is likely affected by the relative expression of the two myosin heavy chain (MyHC) isoforms, namely alpha-MyHC and beta-MyHC. The relative expression of each isoform is regulated developmentally and in pathophysiological states. Many pathophysiological states are associated with small shifts in the relative expression of each MyHC isoform, yet the functional consequence of these shifts remains unclear. The purpose of this study was to determine the functional effect of a small shift in the relative expression of alpha-MyHC. To this end, power output was measured in rat cardiac myocyte fragments that expressed approximately 12% alpha-MyHC and in myocyte fragments that expressed approximately 0% alpha-MyHC, as determined in the same cells by SDS-PAGE analysis after mechanical experiments. Myocyte fragments expressing approximately 12% alpha-MyHC developed approximately 52% greater peak normalized power output than myocyte fragments expressing approximately 0% alpha-MyHC. These results indicate that small amounts of alpha-MyHC expression significantly augment myocyte power output.
Herron
Todd J
TJ
Department of Physiology, University of Missouri School of Medicine, Columbia, MO, USA.
McDonald
Kerry S
KS
D000818:Animals; D001696:Biomechanical Phenomena; D048429:Cell Size / Q000502:physiology; D004591:Electrophoresis, Polyacrylamide Gel; D008297:Male; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D018995:Myosin Heavy Chains / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley
D018995:Myosin Heavy Chains