Telomere length behaves as biomarker of somatic redundancy rather than biological age

Boonekamp, Jelle J.; Simons, Mirre J. P.; Hemerik, Lia; Verhulst, Simon

doi:10.1111/acel.12050

Cited by 192 publications

(190 citation statements)

References 10 publications

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“…Consequently, investigations of human telomeres have controversial results in using telomere length as an accurate biological indicator of age (Mather et al, 2011;Boonekamp et al, 2013). However, in our study, there is a significant correlation between telomere length and hens age from 1 up to 450 days.…”

Section: Discussioncontrasting

confidence: 55%

Age-Dependent Variation of Telomere Length and DNA Damage in Chicken

Makarenko

Усатов

Getmantseva

et al. 2017

OnLine Journal of Biological Sciences

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Abstract:Birds are unique models for molecular studies on aging processes and cellular senescence because of their slow rates of aging and comparatively long life spans among homoeothermic animals. The study aimed to examine the relative telomere length and amount of nuclear, mitochondrial DNA lesions in hens of different ages and to find out the correlation between these biomarkers of aging. The study was carried out on hens of crossbreed «High Sex Brown» of different age groups -1, 75, 225, 330, 450 days old. The measurements of telomeres and DNA damage were done in red cells of hens using quantitative PCR technique. We found out that the amount of telomeric DNA reduced significantly with age. Telomere length ratio to control group (1 day old) made up: 0.88±0.08 for 75 days old, 0.73±0.07 for 225 days old, 0.66±0.1 for 330-days old and 0.58±0.12 for 450 days old. The amount of DNA lesions in both genomes had great, age-dependent increase. The relative quantity of lesions per 10 kb detected in the nuclear DNA were as follows: 0.17±0.19 for 75 days old, 0.66±0.21 for 225 days old, 1.02±0.33 for 330-days old and 1.48±0.45 for 450 days old and the relative quantity of lesions in mtDNA were as follows: 0.11±0.06 for 75 days old, 0.84±0.23 for 225 days old, 1.18±0.3 for 330-days old and 1.49±0.35 for 450 days old. The results obtained are of fundamental interest for aging processes, as well as could have an economic value for poultry farming.

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Section: Discussioncontrasting

confidence: 55%

Age-Dependent Variation of Telomere Length and DNA Damage in Chicken

Makarenko

Усатов

Getmantseva

et al. 2017

OnLine Journal of Biological Sciences

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“…Relatively short telomeres in somatic tissues, as expressed in a shorter LTL, might then reflect diminished somatic reserves with respect to repair capacity. 16,17 Simply put, we propose that a shorter telomere length entails a reduced ability of stem cells to engage in tissue repair, and a component of this tissue repair capacity, represented by telomere length, is determined at birth and during the early years of growth.…”

Section: Circ Cardiovasc Genet February 2015mentioning

confidence: 99%

Association Between Shortened Leukocyte Telomere Length and Cardio-Metabolic Outcomes

Hunt

Kark

Aviv

2015

Circ Cardiovasc Genet

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In their meta-analysis of 27 published studies, D'Mello et al 1 show that shortened leukocyte telomere length (LTL) is associated with 3 primary end points: myocardial infarction, stroke, and type 2 diabetes mellitus. The meta-analysis and its findings raise several fundamental issues that are worth considering. After discussing the major findings and limitations, we focus on 3 central themes: the reliability of LTL measurements, the biological meaning of the association of LTL with cardio-metabolic outcomes, and future directions of telomere research with respect to cardiovascular disease (CVD) and longevity in humans. Article see p 82The underlying reason for meta-analysis is usually lack of consensus across studies. This clearly applies to the field of telomere epidemiology, which is awash with conflicting findings not only in the context of CVD but also cancer and longevity. The meta-analysis of D'Mello et al shows a significant association of LTL with each of the 3 primary end points, but the test for heterogeneity across the studies was significant for each disease. The authors suggest that ethnicity or perhaps demography, which is often associated with ethnicity, might explain some disagreements in findings across populations (and studies). Notably, however, 26 of the 27 studies analyzed across the 3 primary disease end points had odds ratios >1, indicating that the observed heterogeneity resulted from varying magnitudes of a positive association with disease and not from some studies showing inverse associations. The subgroup analysis in Figure 3 of the D'Mello paper suggests that the racial or ethnic group with the highest prevalence of the specific disease showed the smallest association with LTL (Asians for stroke, Hispanics and African Americans for diabetes mellitus). It is unclear why this would be so, unless the higher prevalence of disease in these groups was caused by influential ethnic-related determinants independent of the basic biological and heritable influences of telomere length. The authors were not able to get further data on race and ethnic group from the contributing studies to adequately address these important potentially confounding variables. The number of studies available in some of the racial and ethnic groups was simply too few to draw reliable conclusions as to their influence on the heterogeneity of the estimated disease risks. Also, the inverse association seen in the meta-analysis between sample size and odds ratios estimates (ie, the smaller the study, the more likely the odds ratios estimates were to be elevated) is consistent with the likely publication bias suggested by the authors. Smaller studies with null results are probably unpublished as demonstrated by both Haycock et al and D'Mello et al. Reliability of LTL MeasurementsThe reliability of LTL measurements and sample size are closely linked with respect to findings and conclusions because less reliable LTL measurements require larger samples to test associations and hypotheses. With an interassay coefficient of v...

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“…Telomere shortening can be accelerated by various forms of stress encountered throughout life (Epel et al 2004;Kotrschal et al 2007;Gilley et al 2008;Bauch et al 2013;Boonekamp et al 2014). Short telomeres eventually lead to replicative senescence of the cell (Blackburn 2005), and individuals with longer telomeres have a higher probability of survival in numerous species (Joeng et al 2004;Haussmann et al 2005;Bize et al 2009;Salomons et al 2009), including humans (Boonekamp et al 2013). Furthermore, individual Zebra Finches with longer telomeres at the end of the nestling period have a longer lifespan (Heidinger et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Heritability of telomere length in the Zebra Finch

et al. 2015

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Telomere length predicts survival in birds, and many stressors that presumably reduce fitness have also been linked to telomere length. The response to selection of telomere length will be largely determined by the heritability of this trait; however, little is known about the genetic component of telomere length variation in animals other than humans. Moreover, published heritability estimates of telomere length are based on telomere measurements with techniques that do not distinguish between terminal telomeres, which are susceptible to age and stress, and the interstitial telomeric repeats, which are relatively inert. Heritability estimates that combine interstitial and terminal telomeres are difficult to interpret in species such as birds, where interstitial telomeres are often numerous. We estimated the heritability of terminal telomere length in a captive Zebra Finch population of cross-fostered (half-)siblings using data obtained with an electrophoresis technique that excludes the interstitial repeats from the measurements. We used both a Bayesian quantitative genetic 'animal' model and a frequentist sibling regression approach to estimate heritability. With the animal model, we estimated a high heritability of telomere length (h 2 = 0.99, 95 % credible interval = 0.87-1), but had insufficient statistical power to separate parental and permanent environment effects. The frequentist approach yielded similar heritability estimates, although with large confidence intervals. We used general linear mixed models to disentangle variance components of telomere length. The relative contributions of the individual, mother and father to telomere length variation were statistically indistinguishable at 23-31 %. Chicks were cross-fostered 4-days after hatching, and no effect of rearing nest was found, indicating that any undetected environmental effects exerted their influence prior to, or soon after, hatching. Thus, we conclude that telomere length resemblance between relatives is high and proportional to their relatedness, but we cannot conclusively distinguish between genetic and other forms of inheritance.

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Telomere length behaves as biomarker of somatic redundancy rather than biological age

Cited by 192 publications

References 10 publications

Age-Dependent Variation of Telomere Length and DNA Damage in Chicken

Age-Dependent Variation of Telomere Length and DNA Damage in Chicken

Association Between Shortened Leukocyte Telomere Length and Cardio-Metabolic Outcomes

Heritability of telomere length in the Zebra Finch

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