| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1930456 | Biochemical and Biophysical Research Communications | 2011 | 6 Pages |
Abnormalities in intracellular Ca2+ handing are believed to contribute to arrhythmogenesis during atrial fibrillation (AF). Ca2+/calmodulin-dependent protein kinaseII δ (CaMKIIδ) overexpression was detected in atrial myocytes from patients and animal models with persistent AF. In the present study, we found that rapid electrical field stimulation applied to primary atrial myocytes altered the CaMKIIδ activity, not expression level, resulting in Ca2+ disorder. By lentivirus mediated delivery of CaMKIIδ gene or siRNA into atrial myocytes, cells with different CaMKIIδ expression were generated. Changes of CaMKIIδ expression altered the sarcoplasmic reticulum (SR) Ca2+ release and L-type Ca2+ channels current (ICa) in both steady and electrical stimulating state. These results revealed the important role of CaMKIIδ in Ca2+ disorder caused by electrical field stimulation. It also provided a potential method to improve Ca2+ disorder in AF by modulating CaMKIIδ expression level.
► CaMKIIδ expression in primary atrial myocytes was manipulated by lentiviral vectors mediated gene or siRNA delivery ► Changes of CaMKIIδ expression altered the intracelluar Ca2+ of atrial myocytes. ► Importantly, Ca2+ disorder caused by electrical field stimulation was improved by modulating CaMKIIδ expression.
