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Division of Biostatistics, and the Center for Cardiovascular Research, Departments of Pathology and Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
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.
connexin-deficient mice; confocal immunofluorescence microscopy; electron microscopy; intercalated disks; fascia adherens junctions
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