Tarbiat Modares University Pathobiology Research 2538-3000 20 4 2018 12 01 BACE1-AS non-coding RNA increases apoptosis in HAOEC endothelial cells RNA غیرکدکننده BACE1-AS در سلول‌های اندوتلیال HAOEC و افزایش مرگ سلولی برنامه‌ریزی شده 53 66 19313 EN Majid Sadeghizadeh Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran Iman Sadeghi Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran Babak Bakhshinejad Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran Hossein Moradi Rehabdarkolaee Department of Statistical Sciences and Operations Research, Virginia Commonwealth University, Richmond, VA 23284, U.S.A Majid Sadeghizadeh Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran Journal Article Objective: 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. Methods: 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. Results: 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). Conclusion: 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. https://mjms.modares.ac.ir/article_19313_af5b61bece62a3ec55e911f3ce5e7857.pdf