报告题目:Correlation of genetic and cardiovascular risk markers with blood telomere length–understanding role of telomere in cardiovascular disease
报 告 人:Dr. WANG Xueying,
Assistant Professor and Principal Investigator at Department of Biochemistry, NUS, Singapore
报告时间:2013年5月20日 上午 10：00-11：00
报告地点:生物药学楼1号楼 (大红楼) 105室
Abstract：Telomeres at the ends of chromosomes are critical for maintaining chromosomal stability and cellular genomic integrity. Telomere length (TL) shortens with age and can be accelerated through oxidative stress. Epidemiologic studies have shown that average TL of peripheral blood or buccal DNA, a surrogate biomarker of telomere abnormality, is related to risk of various chronic diseases such as cardiovascular disease (CVD) and cancer, all of which increase in incidence with ageing. Dietary nutrients and genetic factors also influence TL; accelerate TL shortening in some cases. However, the link is not clear and the mechanism is unknown. Using a pilot study of about 500 human blood samples from the Singapore Chinese Health Study (SCHS) with well characterized dietary determinants and known risk markers of CVD already measured in the cohort (e.g., cholesterol levels in hypercholesterolaemia condition of CVD), we performed leukocyte TL association studies. We found TL of participants shortens with increasing chronological age, correlated with literature. Statistical analysis also reveals sexual dimorphism in TL where females had longer mean TL than males. Interestingly, smokers have a significantly shorter TL than non-smokers, which implies an increased exposure to oxidative stress. This is the first report ever in an Asian population with genetic homogeneity from the SCHS. More importantly, TL correlated inversely with cholesterol level and it is mainly with low density lipoprotein, suggesting the development of TL as an early risk marker of CVD. With the pilot 500 samples and employing arrays, chips, and molecular telomere biology techniques, we aim to find detailed link of TL to CVD risk markers and whether this link could be influenced by primary genetic (single nucleotide polymorphisms) and/or secondary (nutrition and dietary determinants) causes of CVD. Finally, we aim to investigate the possible mechanistic pathways involved and thereafter devise appropriate therapeutic agents against CVD risk.