RESUMO
We tested the hypothesis that cardiac allograft dysfunction in acute cardiac rejection may be related, in part, to diminished expression of connexin43, a gap junction channel protein that facilitates intercellular communication 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 evidence of either no rejection or acute cellular rejection. Expression of connexin43 diminished significantly during acute cellular rejection and returned to baseline levels following resolution of rejection. Reversible down-regulation of connexin43 may contribute to ventricular dysfunction in allograft rejection.
