DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age

Research output: Contribution to journalJournal articlepeer-review

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DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age. / Waaijer, Mariëtte E C; Croco, Eleonora; Westendorp, Rudi G J; Slagboom, P Eline; Sedivy, John M; Lorenzini, Antonello; Maier, Andrea B.

In: Aging, Vol. 8, No. 1, 30.01.2016, p. 147-155.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Waaijer, MEC, Croco, E, Westendorp, RGJ, Slagboom, PE, Sedivy, JM, Lorenzini, A & Maier, AB 2016, 'DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age', Aging, vol. 8, no. 1, pp. 147-155. https://doi.org/10.18632/aging.100890

APA

Waaijer, M. E. C., Croco, E., Westendorp, R. G. J., Slagboom, P. E., Sedivy, J. M., Lorenzini, A., & Maier, A. B. (2016). DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age. Aging, 8(1), 147-155. https://doi.org/10.18632/aging.100890

Vancouver

Waaijer MEC, Croco E, Westendorp RGJ, Slagboom PE, Sedivy JM, Lorenzini A et al. DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age. Aging. 2016 Jan 30;8(1):147-155. https://doi.org/10.18632/aging.100890

Author

Waaijer, Mariëtte E C ; Croco, Eleonora ; Westendorp, Rudi G J ; Slagboom, P Eline ; Sedivy, John M ; Lorenzini, Antonello ; Maier, Andrea B. / DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age. In: Aging. 2016 ; Vol. 8, No. 1. pp. 147-155.

Bibtex

@article{b5e2161ae2294ff790851d02de374483,
title = "DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age",
abstract = "The aging process is accompanied by an accumulation of cellular damage, which compromises the viability and function of cells and tissues. We aim to further explore the association between in vitro DNA damage markers and the chronological age of the donor, as well as long-lived family membership and presence of cardiovascular diseases. Therefore, numbers of 53BP1 foci, telomere-associated foci (TAF) and micronuclei were measured in cultured dermal fibroblasts obtained from three age groups of donors (mean age 22, 63 and 90 years). Fibroblasts were cultured without a stressor and with 0.6 μM rotenone for 3 days. We found that 53BP1 foci and TAF were more frequently present in fibroblasts of old donors compared to middle-aged and young donors. No association between micronuclei and donor age was found. Within the fibroblasts of the middle-aged donors we did not find associations between DNA damage markers and long-lived family membership or cardiovascular disease. Results were comparable when fibroblasts were stressed in vitro with rotenone. In conclusion, we found that DNA damage foci of cultured fibroblasts are significantly associated with the chronological age, but not biological age, of the donor.",
author = "Waaijer, {Mari{\"e}tte E C} and Eleonora Croco and Westendorp, {Rudi G J} and Slagboom, {P Eline} and Sedivy, {John M} and Antonello Lorenzini and Maier, {Andrea B}",
note = "PMCID: PMC4761719",
year = "2016",
month = jan,
day = "30",
doi = "10.18632/aging.100890",
language = "English",
volume = "8",
pages = "147--155",
journal = "Aging",
issn = "1945-4589",
publisher = "Impact Journals LLC",
number = "1",

}

RIS

TY - JOUR

T1 - DNA damage markers in dermal fibroblasts in vitro reflect chronological donor age

AU - Waaijer, Mariëtte E C

AU - Croco, Eleonora

AU - Westendorp, Rudi G J

AU - Slagboom, P Eline

AU - Sedivy, John M

AU - Lorenzini, Antonello

AU - Maier, Andrea B

N1 - PMCID: PMC4761719

PY - 2016/1/30

Y1 - 2016/1/30

N2 - The aging process is accompanied by an accumulation of cellular damage, which compromises the viability and function of cells and tissues. We aim to further explore the association between in vitro DNA damage markers and the chronological age of the donor, as well as long-lived family membership and presence of cardiovascular diseases. Therefore, numbers of 53BP1 foci, telomere-associated foci (TAF) and micronuclei were measured in cultured dermal fibroblasts obtained from three age groups of donors (mean age 22, 63 and 90 years). Fibroblasts were cultured without a stressor and with 0.6 μM rotenone for 3 days. We found that 53BP1 foci and TAF were more frequently present in fibroblasts of old donors compared to middle-aged and young donors. No association between micronuclei and donor age was found. Within the fibroblasts of the middle-aged donors we did not find associations between DNA damage markers and long-lived family membership or cardiovascular disease. Results were comparable when fibroblasts were stressed in vitro with rotenone. In conclusion, we found that DNA damage foci of cultured fibroblasts are significantly associated with the chronological age, but not biological age, of the donor.

AB - The aging process is accompanied by an accumulation of cellular damage, which compromises the viability and function of cells and tissues. We aim to further explore the association between in vitro DNA damage markers and the chronological age of the donor, as well as long-lived family membership and presence of cardiovascular diseases. Therefore, numbers of 53BP1 foci, telomere-associated foci (TAF) and micronuclei were measured in cultured dermal fibroblasts obtained from three age groups of donors (mean age 22, 63 and 90 years). Fibroblasts were cultured without a stressor and with 0.6 μM rotenone for 3 days. We found that 53BP1 foci and TAF were more frequently present in fibroblasts of old donors compared to middle-aged and young donors. No association between micronuclei and donor age was found. Within the fibroblasts of the middle-aged donors we did not find associations between DNA damage markers and long-lived family membership or cardiovascular disease. Results were comparable when fibroblasts were stressed in vitro with rotenone. In conclusion, we found that DNA damage foci of cultured fibroblasts are significantly associated with the chronological age, but not biological age, of the donor.

U2 - 10.18632/aging.100890

DO - 10.18632/aging.100890

M3 - Journal article

C2 - 26830451

VL - 8

SP - 147

EP - 155

JO - Aging

JF - Aging

SN - 1945-4589

IS - 1

ER -

ID: 160192274