Volume 20, Issue 4 (2018)
mjms 2018, 20(4): 53-66 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Sadeghi I, Bakhshinejad B, Moradi Rehabdarkolaee H, Sadeghizadeh M. BACE1-AS non-coding RNA increases apoptosis in HAOEC endothelial cells. mjms 2018; 20 (4) :53-66
URL: http://mjms.modares.ac.ir/article-30-6495-en.html
URL: http://mjms.modares.ac.ir/article-30-6495-en.html
1- Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
2- Department of Statistical Sciences and Operations Research, Virginia Commonwealth University, Richmond, VA 23284, U.S.A
2- Department of Statistical Sciences and Operations Research, Virginia Commonwealth University, Richmond, VA 23284, U.S.A
Abstract: (9970 Views)
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.
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.
Keywords: Heart failure, Biomarker, Non-coding RNA
Article Type: Original Manuscipt |
Subject:
Clinical Pathology
Received: 2017/06/30 | Accepted: 2017/09/13
Received: 2017/06/30 | Accepted: 2017/09/13
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |