Key result
The long non-coding RNA AK055347 was significantly upregulated in the pulmonary vein and surrounding left atrial area compared to the left atrial appendage in patients with atrial fibrillation.
Absolute Event Rate: 6.565% vs 5.178%
p-value: p=<0.00001
The lncRNA AK055347 is upregulated in the LA-PV of AF patients and may contribute to AF pathogenesis by regulating mitochondrial energy production.
The role of long non-coding RNAs (lncRNAs) in atrial fibrillation remains to be fully elucidated. The current study performed microarray analysis to investigate differential lncRNA expression profiling in atrial samples from the pulmonary vein and the surrounding left atrial area (LA‑PV) and from the left atrial appendage (LAA) in 16 patients with atrial fibrillation (AF). Microarray analysis identified 94 lncRNAs that were differentially expressed between the LA‑PV and LAA in patients with AF. AK055347 was one of lncRNAs with the most significant alterations observed. Knockdown of AK055347 inhibited cell viability of H9C2 cardiomyocytes, accompanied by downregulation of Cyp450 and ATP synthases. In addition, microarray analysis identified that MSS51 was a target of AK055347. Knockdown of AK055347 inhibited the expression of MSS51 in H9C2 cells. The observations of the current study suggest that lncRNAs are differentially expressed in the LA‑PV and LAA in patients with AF. AK055347 may contribute to the pathogenesis of AF by dysregulating mitochondrial energy production via regulation of Cyp450, ATP synthase and MSS51.
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Chen et al. (2016) studied Atrial fibrillation (n=16). Pulmonary vein and surrounding left atrial area (LA-PV) tissue vs. Left atrial appendage (LAA) tissue was evaluated on AK055347 expression level (p=<0.00001). The long non-coding RNA AK055347 was significantly upregulated in the pulmonary vein and surrounding left atrial area compared to the left atrial appendage in patients with atrial fibrillation.
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