Telomeres shorten at equivalent rates in somatic tissues of adults

Significance This paper makes two contributions to research on the link between the social environment and health. Using data from a birth cohort study, we show that, among African American boys, those who grow up in highly disadvantaged environments have shorter telomeres (at age 9) than boys who grow up in highly advantaged environments. We also find that the association between the social environment and telomere length (TL) is moderated by genetic variation within the serotonin and dopamine pathways. Boys with the highest genetic sensitivity scores had the shortest TL when exposed to disadvantaged environments and the longest TL when exposed to advantaged environments. To our knowledge, this report is the first to document a gene–social environment interaction for TL, a biomarker of stress exposure.

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“…S2 and S3). Our study validates other work showing that multiple tissues, including saliva, can be used to measure TL (16,17).…”

supporting

confidence: 90%

Social disadvantage, genetic sensitivity, and children’s telomere length

Mitchell

Hobcraft

McLanahan

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

244

215

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“…IP address: 35.167.132.9, on 10 May 2018 at 07:13:24, subject to the Cambridge Core terms of use, available at age-dependent telomere shortening is similar across different tissues within an individual, particularly between proliferative (leukocytes) and low proliferative (muscle) tissues (Daniali et al, 2013;Kuznetsova et al, 2010). However, these studies do not address whether the rate of telomere shortening across organs remains similar during disease.…”

Section: Twin Research and Human Geneticsmentioning

confidence: 99%

Does Telomere Shortening Precede the Onset of Hypertension in Spontaneously Hypertensive Mice?

et al. 2016

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Telomere length is widely considered as a marker of biological aging. Clinical studies have reported associations between reduced telomere length and hypertension. The aim of this study was to compare telomere length in hypertensive and normotensive mice at pre-disease and established disease time points to determine whether telomere length differs between the strains before and after the onset of disease. Genomic DNA was extracted from kidney and heart tissues of 4-, 12-, and 20-week-old male hypertensive (BPH/2J) and normotensive (BPN/3J) mice. Relative telomere length (T/S) was measured using quantitative PCR. Age was inversely correlated with telomere length in both strains. In 4-week-old pre-hypertensive animals, no difference in T/S was observed between BPH/2J and BPN/3J animals in kidney or heart tissue (kidney p = 0.14, heart p = 0.06). Once the animals had established disease, at 12 and 20 weeks, BPH/2J mice had significantly shorter telomeres when compared to their age-matched controls in both kidney (12 weeks p < 0.001 and 20 weeks p = 0.004) and heart tissues (12 weeks p < 0.001 and 20 weeks p < 0.001). This is the first study to show that differences in telomere lengths between BPH/2J and BPN/3J mice occur after the development of hypertension and do not cause hypertension in the BPH/2J mice.

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“…Shortening of telomeres occurs in somatic cells during aging (Daniali et al ., 2013) due to DNA damage and incomplete end processing (von Zglinicki et al ., 2000). Above a threshold, telomere erosion results in the arrest of cellular proliferation and the dysfunction of renewable tissues.…”

Section: Introductionmentioning

confidence: 99%

P66SHC deletion improves fertility and progeric phenotype of late-generation TERC-deficient mice but not their short lifespan

2016

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SummaryOxidative stress and telomere attrition are considered the driving factors of aging. As oxidative damage to telomeric DNA favors the erosion of chromosome ends and, in turn, telomere shortening increases the sensitivity to pro‐oxidants, these two factors may trigger a detrimental vicious cycle. To check whether limiting oxidative stress slows down telomere shortening and related progeria, we have investigated the effect of p66SHC deletion, which has been shown to reduce oxidative stress and mitochondrial apoptosis, on late‐generation TERC (telomerase RNA component)‐deficient mice having short telomeres and reduced lifespan. Double mutant (TERC −/− p66SHC −/−) mice were generated, and their telomere length, fertility, and lifespan investigated in different generations. Results revealed that p66SHC deletion partially rescues sterility and weight loss, as well as organ atrophy, of TERC‐deficient mice, but not their short lifespan and telomere erosion.Therefore, our data suggest that p66SHC‐mediated oxidative stress and telomere shortening synergize in some tissues (including testes) to accelerate aging; however, early mortality of late‐generation mice seems to be independent of any link between p66SHC‐mediated oxidative stress and telomere attrition.

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Telomeres shorten at equivalent rates in somatic tissues of adults

Cited by 536 publications

References 36 publications

Social disadvantage, genetic sensitivity, and children’s telomere length

Social disadvantage, genetic sensitivity, and children’s telomere length

Does Telomere Shortening Precede the Onset of Hypertension in Spontaneously Hypertensive Mice?

P66SHC deletion improves fertility and progeric phenotype of late-generation TERC-deficient mice but not their short lifespan

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