Saffitz J E, Green K G, Kraft W J, Schechtman K B, Yamada K A
Division of Biostatistics, and the Center for Cardiovascular Research, Departments of Pathology and Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Am J Physiol Heart Circ Physiol. 2000 May;278(5):H1662-70. doi: 10.1152/ajpheart.2000.278.5.H1662.
Gap junction number and size vary widely in cardiac tissues with disparate conduction properties. Little is known about how tissue-specific patterns of intercellular junctions are established and regulated. To elucidate the relationship between gap junction channel protein expression and the structure of gap junctions, we analyzed Cx43 +/- mice, which have a genetic deficiency in expression of the major ventricular gap junction protein, connexin43 (Cx43). Quantitative confocal immunofluorescence microscopy revealed that diminished Cx43 signal in Cx43 +/- mice was due almost entirely to a reduction in the number of individual gap junctions (226 +/- 52 vs. 150 +/- 32 individual gap junctions/field in Cx43 +/+ and +/- ventricles, respectively; P < 0.05). The mean size of an individual gap junction was the same in both groups. Immunofluorescence results were confirmed with electron microscopic morphometry. Thus when connexin expression is diminished, ventricular myocytes become interconnected by a reduced number of large, normally sized gap junctions, rather than a normal number of smaller junctions. Maintenance of large gap junctions may be an adaptive response supporting safe ventricular conduction.
在具有不同传导特性的心脏组织中，缝隙连接的数量和大小差异很大。关于细胞间连接的组织特异性模式是如何建立和调节的，人们知之甚少。为了阐明缝隙连接通道蛋白表达与缝隙连接结构之间的关系，我们分析了Cx43+/-小鼠，这些小鼠在主要的心室缝隙连接蛋白连接蛋白43（Cx43）的表达上存在基因缺陷。定量共聚焦免疫荧光显微镜显示，Cx43+/-小鼠中Cx43信号的减弱几乎完全是由于单个缝隙连接数量的减少（Cx43+/+和+/-心室中分别为226±52个和150±32个单个缝隙连接/视野；P<0.05）。两组中单个缝隙连接的平均大小相同。免疫荧光结果通过电子显微镜形态计量学得到证实。因此，当连接蛋白表达减少时，心室肌细胞通过数量减少的大的、正常大小的缝隙连接相互连接，而不是正常数量的较小的连接。维持大的缝隙连接可能是一种支持安全心室传导的适应性反应。
