Gordon L, Wharton J, Moore S E, Flanigan T P, Gulbenkian S, Walsh F S, David-Ferreira J F, Winter R J, Polak J M
Department of Histochemistry, Royal Postgraduate Medical School, London, UK.
Life Sci. 1990;47(7):601-9. doi: 10.1016/0024-3205(90)90571-8.
Myocardial neural cell adhesion molecule (N-CAM) is temporally regulated, being expressed during cardiac morphogenesis and innervation and suppressed in the adult heart. We have investigated the plasticity of N-CAM expression in hypertrophic muscle using the rat model of chronic hypoxia to selectively induce right ventricular hypertrophy over a 14 day time course. Sarcolemmal and intercalated disc N-CAM immunostaining was more extensive in the ventricular myocardium of hypoxic rats compared to normoxic controls. Quantitative assessment of the immunoreactivity in tissue extracts demonstrated a selective increase in the amount of N-CAM immunoreactivity in the hypertrophic myocardium of the right ventricle of rats exposed to hypoxia and this was associated with an increase of the 125 kDa isoform. We conclude that myocardial hypertrophy may be a factor influencing N-CAM expression in the heart and adhesion molecules may have a role in cardiac remodelling.
心肌神经细胞黏附分子（N-CAM）受到时间调控，在心脏形态发生和神经支配期间表达，而在成年心脏中受到抑制。我们使用慢性缺氧大鼠模型，在14天的时间进程中选择性诱导右心室肥大，研究了肥厚心肌中N-CAM表达的可塑性。与常氧对照组相比，缺氧大鼠心室心肌中的肌膜和闰盘N-CAM免疫染色更为广泛。对组织提取物中免疫反应性的定量评估表明，暴露于缺氧环境的大鼠右心室肥厚心肌中N-CAM免疫反应性的量有选择性增加，这与125 kDa异构体的增加有关。我们得出结论，心肌肥大可能是影响心脏中N-CAM表达的一个因素，黏附分子可能在心脏重塑中起作用。
