Screening for differential methylation status in fetal myocardial tissue samples with ventricular septal defects by promoter methylation microarrays.
نویسندگان
چکیده
To identify and provide a global assessment of DNA methylation in fetal ventricular septal defect (VSD), genomic DNA extracted from fetal myocardial tissue samples with VSD (n=21) and from normal fetal myocardial tissue samples (n=15) was analyzed for gene methylation using array‑based technology. Furthermore, the KIAA0310, RAB43, SIVA1 and NDRG2 genes were randomly selected for validation analysis using methylation-specific PCR. Our results revealed that 70 and 85 genes were regulated by hypermethylation and hypomethylation, respectively, in VSD. Different clusters of genes were associated with functions including embryo development, signal transduction, cell apoptosis and cell proliferation. In conclusion, this study identified a set of candidate genes whose expression is regulated by DNA methylation in fetal VSD.
منابع مشابه
Analysis of Methylation Status in Promoter Region of Γ- Globin Gene in Carrier and Affected Β-Thalassemia Patients with High Level of Fetal Hemoglobin in Comparison with Normal Individuals
Introduction: Among the factors that may be associated with the re-expression gamma-globin in adults is the methylation pattern of the promoter region. The study aimed to determine the association between promoter methylation pattern of the gamma-globin gene in the carriers and affected beta-thalassemia individuals and its expression levels. Methods: This study has been done as a case control-...
متن کاملTwo Steps Methylation Specific PCR for Assessment of APC Promoter Methylation in Gastric Adenocarcinoma
Gastric Cancer (GC) is the second most common cancer in the world and a leading cause of cancer-related mortality. Methylation of promoter CpG islands (CGIs) belonging to tumor suppressor genes causes transcriptional silencing of their corresponding genes leading to carcinogenesis and other disorders. Adenomatous Polyposis Coli (APC) a tumor suppressor gene is inactivated by methylation of prom...
متن کاملE-cadherin Promoter Methylation Comparison and Correlation with the Pathological Features of the Squamous Cell Carcinoma of Esophagus in the High Risk Region
E-cadherin is among tumor suppressor genes which mostly subjects to the down-regulation in squamous cell carcinoma of esophagus (SCCE). The gene is tightly associated with the tumor invasion and metastasis in multiple human cancers, especially SCCE. CpG islands’ methylation in the promoter region of E-cadherin is among the mechanisms that have been suggested for the E-cadherin silencing, howeve...
متن کاملStudy of the role of siRNA mediated promoter methylation in DNMT3B knockdown and alteration of promoter methylation of CDH1, GSTP1 genes in MDA-MB -453 cell line
Promoter methylation is one of the main epigenetic mechanisms that lead to the inactivation of tumor suppressor genes during carcinogenesis. Due to the reversible nature of DNA methylation, many studies have been performed to correct theses epigenetic defects by inhibiting DNA methyltransferases (DNMTs). In this case novel therapeutics especially siRNA oligonucleotides have been used to specifi...
متن کاملهایپومتیلاسیون DNA در پروموتر ژن (NR5A1) nuclear receptor subfamily 5 group A member1 مرتبط با اندومتریوز زنان در شمال غرب ایران
Background and objectives: Endometrial tissue growth and its activity outside the uterus cause endometriosis. It has been suggested that various epigenetic deviations play a major role in the pathogenesis of endometriosis. Steroidogenic factor 1 (SF-1; NR5A1) is an essential transcription factor for estrogen biosynthesis in endometrial cells. The expression of SF-1 in endometriosis and lack of ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Molecular medicine reports
دوره 4 1 شماره
صفحات -
تاریخ انتشار 2011