Xizhe Zhao1,2, Yi Li3, Yan Yan4, Xuelian Ma4, Caixia Guo5. 1. Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, 119# Nansihuanxilu, Fentai District, Beijing, 100070, China. 2. Department of Cardiology, Beijing Electric Power Hospital, Beijing, China. 3. Department of Clinical Laboratory, Beijing Electric Power Hospital, Beijing, China. 4. Department of Physical Examination, Beijing Electric Power Hospital, Beijing, China. 5. Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, 119# Nansihuanxilu, Fentai District, Beijing, 100070, China. cxgbb@163.com.
Abstract
BACKGROUND: ACS (acute coronary syndrome), a subgroup of coronary artery disease (CHD), is a leading cause of death worldwide. Reports shown the association between methylation and CHD, while the abnormal expression of C1QTNF1 (C1q and tumor necrosis factor related protein 1) in CHD patients, but the underlying mechanisms are still unclear. OBJECTIVE: To analyze the methylation of CpG sites of C1QTNF1 in ACS patients. METHODS: Peripheral blood samples were collected from healthy controls and ACS patients. The methylation of total C1QTNF1, promoter sequence and CpG sites of C1QTNF1 were measured using methylation detection kits. The outcomes were compared between patients and controls based on gender, clinical classification and clinical stages. RESULTS: The promoter sequences from 37 ACS patients and 20 controls indicate that the methylation rate of C1QTNF1 was significantly lower in male patients compared to healthy controls at + 63 CpG sites (p = 0.03). Whereas, the methylation rate of C1QTNF1 in female patients was significantly lower than female health controls at - 89, + 39 and + 167 CpG sites (p = 0.021, 0.042, 0.021). In addition, the methylation rate of C1QTNF1 was significantly higher in male patients than female patients at - 89, - 41 and + 39 CpG sites (p = 0.011, 0.043, 0.006). Moreover, the methylation rate significantly decreased at - 24 sites (p = 0.021), but it significantly increased at - 14 site (p = 0.048) in patients with UA, compared to patients with STEMI (ST-segment elevation myocardial infarction). CONCLUSIONS: There were significant differences in the methylation rate + 63 CpG sites between controls and male ACS patients. The - 14 site methylation increased in patients with UA, compared to patients with STEMI.
BACKGROUND: ACS (acute coronary syndrome), a subgroup of coronary artery disease (CHD), is a leading cause of death worldwide. Reports shown the association between methylation and CHD, while the abnormal expression of C1QTNF1 (C1q and tumor necrosis factor related protein 1) in CHD patients, but the underlying mechanisms are still unclear. OBJECTIVE: To analyze the methylation of CpG sites of C1QTNF1 in ACS patients. METHODS: Peripheral blood samples were collected from healthy controls and ACS patients. The methylation of total C1QTNF1, promoter sequence and CpG sites of C1QTNF1 were measured using methylation detection kits. The outcomes were compared between patients and controls based on gender, clinical classification and clinical stages. RESULTS: The promoter sequences from 37 ACS patients and 20 controls indicate that the methylation rate of C1QTNF1 was significantly lower in male patients compared to healthy controls at + 63 CpG sites (p = 0.03). Whereas, the methylation rate of C1QTNF1 in female patients was significantly lower than female health controls at - 89, + 39 and + 167 CpG sites (p = 0.021, 0.042, 0.021). In addition, the methylation rate of C1QTNF1 was significantly higher in male patients than female patients at - 89, - 41 and + 39 CpG sites (p = 0.011, 0.043, 0.006). Moreover, the methylation rate significantly decreased at - 24 sites (p = 0.021), but it significantly increased at - 14 site (p = 0.048) in patients with UA, compared to patients with STEMI (ST-segment elevation myocardial infarction). CONCLUSIONS: There were significant differences in the methylation rate + 63 CpG sites between controls and male ACS patients. The - 14 site methylation increased in patients with UA, compared to patients with STEMI.