Myosin isoenzymes in human hypertrophic hearts. Shift in atrial myosin heavy chains and in ventricular myosin light chains

Abstract

(J Clin Invest 1982; 69: 816-825

Proteomic Analysis of Pharmacologically Preconditioned Cardiomyocytes Reveals Novel Phosphorylation of Myosin Light Chain 1

“…26 In addition, a number of cases of altered MLC1 ventricular expression in chronic cardiovascular disease states may be associated with significant functional consequences. Hypertrophied left ventricles of patients with ischemic, dilated, and hypertrophic cardiomyopathy express small amounts of atrial MLC1, [27][28][29] not normally present in the adult ventricle. Postsurgical return to a normal hemodynamic state decreased this ventricular expression of atrial MLC1.…”

Designing Heart Performance by Gene Transfer

“…Permeabilized fiber studies from these mice showed a change in cardiac fiber function such that the incorporation of either ELC1 v or RLC2 v into atrial fibers caused decreased unloaded shortening velocity (787). Interestingly, myosin light-chain isoform switching, where the ventricular isoforms convert to the atrial light chains, has been documented in various human heart failure cases such as in congestive heart failure or in DCM (26, 601,794), suggesting important and divergent physiological roles in cardiac muscle for the ventricular versus atrial myosin light chains. The precise role of the different cardiac muscle MLC isoforms in cardiac function is not fully known.…”

Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies

“…Therefore, this protein has been designated the embryonic myosin light chain (MLC) (16). The expression of this isoform was detected in the hypertrophied human ventricle (17). The hypertrophied right ventricle of children with tetralogy of Fallot (18) and the hemodynamically overloaded left ventricle of patients with valvular disease (19,20) also express a large amount of ALC 1 .…”

“…Although ALC 1 becomes re-expressed in the overloaded human ventricle (17,19,20,22,74), β-MHC may combine with either ALC 1 and/or ventricular light chain 1 (VLC 1 ) to form two homodimers and one heterodimer in diseased human ventricles (23). The main consequence of ALC 1 re-expression in the ventricle is the increase of Ca 2+ sensitivity of the contractile apparatus (74).…”