Elham Taheri Bajgan - Molecular Genetics Department, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
Ali Zahedmehr - Cardiovascular Intervention Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
Farshad Shakerian - Cardiogenetic Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
Majid Maleki - Cardiogenetic Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
Mahshid Malakootian - Cardiogenetic Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
Seyed Javad Mowla - Molecular Genetics Department, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran

Background and Aim: Coronary artery disease (CAD) is the most common cause of death in industrialized countries and is rapidly increasing in prevalence in developing countries. Despite current therapeutic strategies which focus on modifying lifestyle risk factors, recent genetic studies have introduced many loci associated with CAD. A specific age group of CAD patients are attributed as premature-CAD; women under ۵۰ and men under ۴۰ years old. Premature-CAD seems to rely more on genetic factors rather than environmental causes. The ۹p۲۱.۳ locus is the most influential genetic risk factor for CAD. ANRIL non-coding RNA is encoded from this region and is highly related to CAD both in expression alteration and genetic variation level.Methods: In this study we aimed to investigate the expression pattern of ANRIL exons in premature CAD patients. Serum samples of patients were collected before angiography. RNA extraction and concentration were performed using QIAGEN and Norgen kits respectively. The expression of ANRIL exons was assessed by real-time PCR. Statistical analysis was performed using GraphPad prism ۶ software.Results: Using different sets of specific primers for both internal and terminal exons, we identified different expression patterns between CAD and non-CAD groups. Downregulation of ANRIL was significantly detected in CAD samples when using specific primers amplifying first exons while changing primers to medial and ۳’ exons altered the aforementioned observation.Conclusion: Altogether, differential expression of ANRIL exons in serum samples of patients suffering from premature CAD may be due to the presence of different ANRIL spliced variants in serum, reflecting the circulating content of transcriptome.

ANRIL, premature CAD, Serum