Histone acetylation during aging of human cells in culture

Ryan, Jon M.; Cristofalo, Vincent J.

doi:10.1016/0006-291x(72)90668-7

Cited by 76 publications

(20 citation statements)

References 11 publications

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“…In another study, the acetylation of H4K5, but not total H4, was shown to decrease with age in C.elegans , and longevity could be extended with an HDAC inhibitor [60]. A global reduction in H4 acetylation has also been observed in rat cerebral cortex neurons and cultured human cells [76]. H4K20 trimethylation levels are found to increase with increasing age in human tissues and HGPS cells [77].…”

Section: Epigenetic Misregulation Dna Repair and Aging: An Emerging mentioning

confidence: 99%

‘Relax and Repair’ to restrain aging

Krishnan

Liu

Zhou

2011

Aging

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The maintenance of genomic integrity requires the precise identification and repair of DNA damage. Since DNA is packaged and condensed into higher order chromatin, the events associated with DNA damage recognition and repair are orchestrated within the layers of chromatin. Very similar to transcription, during DNA repair, chromatin remodelling events and histone modifications act in concert to ‘open’ and relax chromatin structure so that repair proteins can gain access to DNA damage sites. One such histone mark critical for maintaining chromatin structure is acetylated lysine 16 of histone H4 (AcH4K16), a modification that can disrupt higher order chromatin organization and convert it into a more ‘relaxed’ configuration. We have recently shown that impaired H4K16 acetylation delays the accumulation of repair proteins to double strand break (DSB) sites which results in defective genome maintenance and accelerated aging in a laminopathy-based premature aging mouse model. These results support the idea that epigenetic factors may directly contribute to genomic instability and aging by regulating the efficiency of DSB repair. In this article, the interplay between epigenetic misregulation, defective DNA repair and aging is discussed.

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Section: Epigenetic Misregulation Dna Repair and Aging: An Emerging mentioning

confidence: 99%

‘Relax and Repair’ to restrain aging

Krishnan

Liu

Zhou

2011

Aging

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“…The functional significance of these proteins is un clear. The rate of histone acetylation decreased between phase II and phase III WI-38 cells (Ryan and Cristofalo, 1972), but this may have been an effect of the decline in the growth rate of late passage cultures, since a rise in histone acetylation correlated with the preparation for cell division (Ryan and Cristofalo, 1972). A simi!…”

Section: Changes In Chromatin Compositionmentioning

confidence: 99%

“…This latter Pochran et al (1978) observation suggests that logarithmically grow ing phase III cultures are similar to 'quiescent' phase II cultures, and contain a large propor tion of 'non-dividing' cells. In Wl-38 cells, the histone:DNA ratio of isolated chromatin has been found to either increase (Srivastava, 1973) or remain constant (Ryan and Cristofalo, 1972) during the in vitro lifespan. Qualitative dif ferences have been reported between chromo somal proteins extracted by salt from phase II and phase III cultures (Maizel et al.…”

Section: Changes In Chromatin Compositionmentioning

confidence: 99%

<i>In vitro</i> ‘Ageing’ and Nuclear Template Function

Whatley¹,

Hill²

1980

Gerontology

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The fundamental cause(s) of senescent deterioration remain(s) to be established. Numerous attempts have been made to relate changes found at the cellular level with altered or failing functional changes occurring at the molecular level. However, the apparently contradictory published data often make it very difficult if not impossible, to decide whether any conclusive evidence has been provided. In this article, we have reviewed the attempts to relate in vitro ‘ageing’ with alterations in nuclear template function and have made brief mention of the few complementary in vivo experiments. Results from studies of chromatin function during in vitro ‘ageing’ in general favour the suggestion that the reduction in template activity with increasing ‘age’ may result from the loss of cellular division potential, so being an effect rather than a cause of in vitro ‘ageing’. However, nuclear control of ‘ageing’ via specific transcript ional mechanisms cannot be excluded by these data. It is possible that minor or discrete species of RNA are involved, but their investigation and detection await the development of new or more sensitive methodologies. Therefore, published data are consistent with theories of genetically programmed cellular senescence and terminal differentiation, but they do not allow us to decide firmly in favour of one or the other.

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“…It is well known that acetylation of histone proteins in cultured human fibroblasts decreases during aging, which is believed to be directly related to decreased metabolic rate and reproductive capacity associated with aging [4]. However, histone deacetylation is not likely to be a universal driving force of aging because histone acetylation and deacetylation mimetics similarly shortened life span [5], which could simply reflect nonspecific fitness decreases in both instances.…”

mentioning

confidence: 99%