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Epigenetic hereditary transcription profiles II, aging revisited.

ABSTRACT: BACKGROUND: Previously, we have shown that deviations from the average transcription profile of a group of functionally related genes can be epigenetically transmitted to daughter cells, thereby implicating nuclear programming as the cause. As a first step in further characterizing this phenomenon it was necessary to determine to what extent such deviations occur in non-tumorigenic tissues derived from normal individuals. To this end, a microarray database derived from 90 human donors aged between 22 to 87 years was used to study deviations from the average transcription profile of the proteasome genes. RESULTS: Increase in donor age was found to correlate with a decrease in deviations from the general transcription profile with this decline being gender-specific. The age-related index declined at a faster rate for males although it started from a higher level. Additionally, transcription profiles from similar tissues were more alike than those from different tissues, indicating that deviations arise during differentiation. CONCLUSION: These findings suggest that aging and differentiation are related to epigenetic changes that alter the transcription profile of proteasomal genes. Since alterations in the structure and function of the proteasome are unlikely, such changes appear to occur without concomitant change in gene function. These findings, if confirmed, may have a significant impact on our understanding of the aging process.

SUBMITTER: Simons JW

PROVIDER: S-EPMC2265679 | biostudies-literature | 2007

REPOSITORIES: biostudies-literature

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Epigenetic hereditary transcription profiles II, aging revisited.

Simons Johannes Wim JW

Biology direct 20071228

<h4>Background</h4>Previously, we have shown that deviations from the average transcription profile of a group of functionally related genes can be epigenetically transmitted to daughter cells, thereby implicating nuclear programming as the cause. As a first step in further characterizing this phenomenon it was necessary to determine to what extent such deviations occur in non-tumorigenic tissues derived from normal individuals. To this end, a microarray database derived from 90 human donors age ...[more]

PMID: 18163906

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Project description:OBJECTIVE:Major depressive disorder is associated with an increased risk of mortality and aging-related diseases. The authors examined whether major depression is associated with higher epigenetic aging in blood as measured by DNA methylation (DNAm) patterns, whether clinical characteristics of major depression have a further impact on these patterns, and whether the findings replicate in brain tissue. METHOD:DNAm age was estimated using all methylation sites in blood of 811 depressed patients and 319 control subjects with no lifetime psychiatric disorders and low depressive symptoms from the Netherlands Study of Depression and Anxiety. The residuals of the DNAm age estimates regressed on chronological age were calculated to indicate epigenetic aging. Major depression diagnosis and clinical characteristics were assessed with questionnaires and psychiatric interviews. Analyses were adjusted for sociodemographic characteristics, lifestyle, and health status. Postmortem brain samples of 74 depressed patients and 64 control subjects were used for replication. Pathway enrichment analysis was conducted using ConsensusPathDB to gain insight into the biological processes underlying epigenetic aging in blood and brain. RESULTS:Significantly higher epigenetic aging was observed in patients with major depression compared with control subjects (Cohen's d=0.18), with a significant dose effect with increasing symptom severity in the overall sample. In the depression group, epigenetic aging was positively and significantly associated with childhood trauma score. The case-control difference was replicated in an independent data set of postmortem brain samples. The top significantly enriched Gene Ontology terms included neuronal processes. CONCLUSIONS:As compared with control subjects, patients with major depression exhibited higher epigenetic aging in blood and brain tissue, suggesting that they are biologically older than their corresponding chronological age. This effect was even more profound in the presence of childhood trauma.

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Epigenetic hereditary transcription profiles II, aging revisited.

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Epigenetic hereditary transcription profiles II, aging revisited.

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