Correlated expression of atrial myosin heavy chain and regulatory light chain isoforms with pressure overload hypertrophy in the non-human primate

Abstract

There is tight coupling between the expression of myosin subunit isoforms under pathological conditions from a primate species closely related to humans. The data suggest that the synthesis of these subunits of myosin may be coordinated at the molecular level.

Effects of Total Replacement of Atrial Myosin Light Chain-2 With the Ventricular Isoform in Atrial Myocytes of Transgenic Mice

“…13,17 On the basis of the present studies, the postnatal MLC isoform switch in the left ventricle of the neonate may facilitate ejection against the increased systemic arterial pressure that occurs at parturition. In addition, several studies have demonstrated expression of the ventricular isoform of MLC2 in the atria of hypertrophied hearts of both humans and experimental animals in response to pathological conditions.…”

“…In addition, several studies have demonstrated expression of the ventricular isoform of MLC2 in the atria of hypertrophied hearts of both humans and experimental animals in response to pathological conditions. [13][14][15][16][17] Wanker et al 15 found MLC2v in atrial samples from patients with a variety of cardiomyopathies, and the level of ventricular isoform expression correlated with the severity of heart failure. Likewise, Cummins 16 reported that the degree of pressure-overload hypertrophy in humans is the most significant factor influencing ventricular MLC2v isoform expression in the human atria.…”

“…A similar phenomenon has been reported in experimental and clinical cardiomyopathies. [13][14][15][16][17] For instance, Kumar et al 13 reported mRNA expression of MLC2v in the atria of the spontaneously hypertensive rat, and an increase in MLC2v protein has been reported in the atria of humans with various cardiomyopathies. 15,16 Because the atria and ventricles of the heart play much different roles in cardiac function (the ventricles are required to generate much greater forces per beat than the atria), we hypothesized that replacement of the atrial isoform with the ventricular species would result in functional changes at the myocyte level.…”

Transgenic Mice with Cardiac-Specific Expression of Activating Transcription Factor 3, a Stress-Inducible Gene, Have Conduction Abnormalities and Contractile Dysfunction

“…Consistent with this notion, TG1 ventricles had significant down-regulation of myosin light chain 2 ventricular isoform (MLC2V) (63 Ϯ 19 versus 100 Ϯ 17, P ϭ 0.0116), a down-regulation also observed in tissues from hypertrophic human hearts and in hypertrophic and hypertensive primate and rodent models. [25][26][27][28] SERCA2a, a marker of heart failure 29 -31 was not significantly different in the ventricles or atria of either line. It is apparent from the literature that different patterns of dysregulation for hypertrophic markers characterize specific murine models; importantly, although some markers may not be up-regulated in specific models, an increase in ␣-skeletal actin is always observed.…”

Progressive Proteome Changes in the Myocardium of a Pig Model for Duchenne Muscular Dystrophy

“…Although the complete functional pattern of this protein remains unclear, it is supposed that MYL7 is a player in cardiac development and contractility. In baboons, levels of ALC-2 expression were shown to be correlated to the expression levels of MHC-alpha in the atrial myocardium (Henkel et al, 1993). Strikingly, the abundance alteration of MYL7 switched during the development of the DMD pigs.…”