Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 278, Issue 5, Pages H1662-H1670Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2000.278.5.H1662
Keywords
connexin-deficient mice; confocal immunofluorescence microscopy; electron microscopy; intercalated disks; fascia adherens junctions
Funding
- NHLBI NIH HHS [HL-58507, HL-50598] Funding Source: Medline
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Gap junction number and size vary widely in cardiac tissues with disparate conduction propel-ties. 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.
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