We tested the hypothesis that cardiac allograft dysfunction in acute cardia
c rejection may be related, in part, to diminished expression of connexin43
, a gap junction channel protein that facilitates intercellular communicati
on and coordinates electrical and mechanical cardiac function. We measured
connexin43 levels using quantitative confocal immunofluorescence microscopy
of endocardial biopsies from heart transplant recipients with histologic e
vidence of either no rejection or acute cellular rejection. Expression of c
onnexin43 diminished significantly during acute cellular rejection and retu
rned to baseline levels following resolution of rejection. Reversible down-
regulation of connexin43 may contribute to ventricular dysfunction in allog
raft rejection.