title: Telomere attrition in white blood cell correlating with cardiovascular damage.
abstract: Aging is a major risk factor for cardiovascular disease. Chronological aging does not always parallel biological aging, but there is no reliable biomarker for the latter. In the present study, we tested the hypothesis that telomere attrition in white blood cells is related to endothelial dysfunction and the extent of atherosclerosis, and thus may serve as a useful marker for biological aging. We evaluated telomere lengths in white blood cells by measuring the mean telomere restriction fragment length (mTRFL), as well as endothelial function by flow mediated dilatation (FMD) in the brachial artery, in patients with various degrees of cardiovascular damage and in normal subjects. Cardiovascular damage was assessed by a cardiovascular damage (CVD) score, with 1 point being given for the presence of each cardiovascular risk factor (hypertension, hyperlipidemia and diabetes) and for each event (angina, myocardial infarction, cerebrovascular event and peripheral vascular disease). Subset analysis of CVD score groups revealed that mTRFL and FMD decreased in the rank order of CVD score. Although mTRFL was inversely correlated with age, telomere index, defined as the ratio of TRFL to TRFL predicted by age, also decreased with increase in CVD score. These results indicate that telomere attrition in white blood cells is more closely associated with endothelial damage and atherosclerosis than is chronological aging, supporting the hypothesis that mTRFL in white blood cells is a useful marker for biological aging of the cardiovascular system.
authors.affiliation: Department of Clinical Laboratory Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.
authors.forename: Hidekatsu
authors.initials: H
authors.lastname: Nakashima
authors.forename: Ryoji
authors.initials: R
authors.lastname: Ozono
authors.forename: Chizuko
authors.initials: C
authors.lastname: Suyama
authors.forename: Taijiro
authors.initials: T
authors.lastname: Sueda
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kambe
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Oshima
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000235:genetics; D015139:Blotting, Southern; D001916:Brachial Artery / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000097:blood* / Q000235:genetics* / Q000503:physiopathology; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D007962:Leukocytes; D008297:Male; D008875:Middle Aged; D012150:Polymorphism, Restriction Fragment Length; D015203:Reproducibility of Results; D012307:Risk Factors; D016615:Telomere; D014664:Vasodilation