| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Outline of Final Research Achievements |
Atrial fibrillation (AF) begets AF in part due to atrial remodeling. This study was to identify microRNA(s) responsible for electrical remodeling in AF. We identified 39 microRNAs differentially expressed in AF patient’s atria, including miR-30d as a candidate responsible for ion channel remodeling by in silico analysis. MiR-30d was significantly up-regulated in cardiomyocytes from AF patients, whereas the mRNA and protein levels of CACNA1C/Cav1.2 and KCNJ3/Kir3.1, postulated targets of miR-30d, were markedly reduced. KCNJ3/Kir3.1 expression was down-regulated by transfection of miR-30 precursor, concomitant with a reduction of the acetylcholine-sensitive inward-rectifier K+ current (IK.ACh). KCNJ3/Kir3.1 expression was enhanced by the knockdown of miR-30d. The downward remodeling of IK.ACh is attributed, at least in part, to deranged Ca2+ handling, leading to the up-regulation of miR-30d in human AF, revealing a novel post-transcriptional regulation of IK.ACh.
|
