BACE1-AS non-coding RNA increases apoptosis in HAOEC endothelial cells

Heart failure is one of the most common types of cardiac diseases with high rate of morbidity and mortality, which places a large burden on society. Despite well care system, the survival rate for end-stage heart failure patients is less than 1%. Several studies have recently shown a significant association between long non-coding RNAs with different cardiac diseases.
We investigated the functional mechanism of BACE1-AS, which was previously reported to be up-regulated in heart failure patients, by assessments of gene expression analysis, cell proliferation, and apoptosis.
BACE1-AS down-regulation significantly reduced expressions of cyclin inhibitors that included CDKN1A, CDKN1B, CDKN1C, CDKN2A, and CDKN2B with the exception of CDKN2C and CDKN2D. BACE1-AS over-expression increased expressions of these cell cycle genes, which implied an effect of BACE1-AS LncRNA on the cell cycle. BACE1-AS down-regulation decreased BCL-2 mRNA expression and increased BAX gene expression. BACE1-AS up-regulation increased BCL-2 and reduced BAX expressions. We did not observe any significant change in cell proliferation with BACE1-AS down-regulation, while BACE1-AS up-regulation decreased cell numbers and induced apoptosis compared with the control group (cells treated with an empty vector).
These results showed the important role of BACE1-AS in cell death and, accordingly, pathogenesis of heart failure. It could be considered a potential biomarker for targeting and treatment of heart failure.