Down-regulation of L-type calcium channel and sarcoplasmic reticular Ca2+-ATPase mRN in human atrial fibrillation without significant change in the mRN of ryanodine receptor, calsequestrin and phospholamban : An insight into the mechanism of atrial electr

OBJECTIVES We investigated the gene expression of calcium-handling genes including L-type calcium channel, sarcoplasmic reticular calcium adenosine triphosphatase (Ca2+-ATPase), ryanodine receptor, calsequestrin and phospholamban in human atrial fibrillation. BACKGROUND Recent studies have demonstrated that atrial electrical remodeling in atrial fibrillation is associated with intracellular calcium overload. However, the changes of calcium-handling proteins remain unclear. METHODS total of 34 patients undergoing open heart surgery were included. Atrial tissue was obtained from the right atrial free wall, right atrial appendage, left atrial free wall and left atrial appendage, respectively. The messenger ribonucleic acid (mRNA) amount of the genes was measured by reverse transcription–polymerase chain reaction and normalized to the mRN levels of glyceraldehyde 3-phosphate dehydrogenase. RESULTS The mRN of L-type calcium channel and of Ca2+-ATPase was significantly decreased in patients with persistent atrial fibrillation for more than 3 months (0.36 ± 0.26 vs. 0.90 ± 0.88 for L-type calcium channel; 0.69 ± 0.42 vs. 1.21 ± 0.68 for Ca2+-ATPase; both p < 0.05, all dat in arbitrary unit). We further demonstrated that there was no spatial dispersion of the gene expression among the four atrial tissue sampling sites. Age, gender and underlying cardiac disease had no significant effects on the gene expression. In contrast, the mRN levels of ryanodine receptor, calsequestrin and phospholamban showed no significant change in atrial fibrillation. CONCLUSIONS L-type calcium channel and the sarcoplasmic reticular Ca2+-ATPase gene were down-regulated in atrial fibrillation. These changes may be consequence of, as well as contributory factor for, atrial fibrillation.