TY - JOUR
T1 - Isozymic changes in myosin of human atrial myocardium induced by overload. Immunohistochemical study using monoclonal antibodies
AU - Tsuchimochi, H.
AU - Sugi, M.
AU - Kuro-o, M.
PY - 1984
Y1 - 1984
N2 - An immunohistochemical study using monoclonal antibodies specific for the heavy chains of either human atrial (HCα) or ventricular (HCβ) myosin was performed to clarify the distribution of each isozyme in normal as well as pressure-overload human hearts. In normal human ventricles, all muscle fibers were stained by a monoclonal antibody (HMC14) specific for HCβ, whereas a small number of fibers reacted with a monoclonal antibody (CMA19) specific for HCα. In contrast, in normal human atria, almost all muscle fibers were stained by CMA19, and a relatively larger number of muscle fibers also reacted with HMC14. Furthermore, in pressure-overloaded atria, muscle fibers reactive with HMC14 were strikingly increased while those reactive with CMA19 showed a corresponding decrease. The extent of this isozymic redistribution was in good correlation with atrial pressure. These results not only confirmed the existence of isoforms of myosin heavy chain in human hearts, but also demonstrated that redistribution of isomyosins could occur as an adaptation to pressure overload.
AB - An immunohistochemical study using monoclonal antibodies specific for the heavy chains of either human atrial (HCα) or ventricular (HCβ) myosin was performed to clarify the distribution of each isozyme in normal as well as pressure-overload human hearts. In normal human ventricles, all muscle fibers were stained by a monoclonal antibody (HMC14) specific for HCβ, whereas a small number of fibers reacted with a monoclonal antibody (CMA19) specific for HCα. In contrast, in normal human atria, almost all muscle fibers were stained by CMA19, and a relatively larger number of muscle fibers also reacted with HMC14. Furthermore, in pressure-overloaded atria, muscle fibers reactive with HMC14 were strikingly increased while those reactive with CMA19 showed a corresponding decrease. The extent of this isozymic redistribution was in good correlation with atrial pressure. These results not only confirmed the existence of isoforms of myosin heavy chain in human hearts, but also demonstrated that redistribution of isomyosins could occur as an adaptation to pressure overload.
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U2 - 10.1172/JCI111466
DO - 10.1172/JCI111466
M3 - Article
C2 - 6746912
AN - SCOPUS:0021194132
SN - 0021-9738
VL - 74
SP - 662
EP - 665
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 2
ER -