title: Increased expression of atrial myosin light chain 1 in the overloaded human left ventricle: possible expression of fetal type myocytes.
abstract: We examined the isoforms of myosin light chain 1 in the human left ventricles using pyrophosphate and sodium dodecyl sulfate polyacrylamide gel electrophoresis, peptide mapping, and immunoblotting with monoclonal antibodies against human atrial light chain 1. The relationship between hemodynamic parameters and light chain 1 isoform composition was compared among groups of patients with hypertrophic cardiomyopathy (n = 8), dilated cardiomyopathy (n = 9) and aortic stenosis (n = 5), and controls (n = 6). (1) The light chain 1, which differed from ventricular light chain 1 found in the normal adult ventricle, was highly expressed in the overload left ventricle, and was identical to atrial and fetal ventricular light chain 1 with respect to the physiochemical and immunological properties. (2) The expression of atrial/fetal light chain 1 was augmented in the subendocardial area in comparison with the mid- or subepicardial areas in the hypertrophied left ventricles. (3) The values (%) of the relative expression of atrial/fetal light chain 1 to total light chains 1 determined by densitometric analysis were significantly higher in patients with dilated cardiomyopathy (40.2 +/- 5.8) and those with aortic stenosis (43.1 +/- 6.2) than in the controls (16.9 +/- 2.5) (p less than 0.01), but there was no significant difference between the patients with hypertrophic cardiomyopathy (28.0 +/- 3.7) and the controls. (4) The values of the ratio significantly correlated with those of peak circumferential wall stress (r = 0.53, p less than 0.005). These results suggest that atrial/fetal light chain 1 is expressed in the left ventricles in response to the increased hemodynamic load.
authors.affiliation: Division of Cardiology, Kumamoto University Medical School, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Nakao
authors.forename: H
authors.initials: H
authors.lastname: Yasue
authors.forename: K
authors.initials: K
authors.lastname: Fujimoto
authors.forename: K
authors.initials: K
authors.lastname: Okumura
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Hitoshi
authors.forename: T
authors.initials: T
authors.lastname: Murohara
authors.forename: K
authors.initials: K
authors.lastname: Takatsu
authors.forename: E
authors.initials: E
authors.lastname: Miyamoto
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D001024:Aortic Valve Stenosis / Q000175:diagnosis / Q000473:pathology* / Q000503:physiopathology; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis / Q000473:pathology* / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000175:diagnosis / Q000473:pathology* / Q000503:physiopathology; D004591:Electrophoresis, Polyacrylamide Gel; D005069:Evaluation Studies as Topic; D005260:Female; D005333:Fetus / Q000166:cytology*; D006352:Heart Ventricles / Q000737:chemistry*; D006439:Hemodynamics; D006801:Humans; D015151:Immunoblotting; D007124:Immunoenzyme Techniques; D007536:Isomerism; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000166:cytology / Q000196:embryology*; D018994:Myosin Light Chains; D043263:Myosin-Light-Chain Phosphatase; D009218:Myosins / Q000737:chemistry*; D010449:Peptide Mapping; D010749:Phosphoprotein Phosphatases / Q000737:chemistry*
chemical_list: D000911:Antibodies, Monoclonal; D018994:Myosin Light Chains; C076659:myosin light chain I; D010749:Phosphoprotein Phosphatases; D043263:Myosin-Light-Chain Phosphatase; D009218:Myosins