Evidence for a role of human blood-borne factors in mediating age-associated changes in molecular circadian rhythms
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View abstract on PubMed
Summary
This summary is machine-generated.Aging alters circadian rhythms through blood-borne factors. Old serum disrupts gene expression related to oxidative phosphorylation and Alzheimer's disease, while increasing cholesterol biosynthesis gene rhythms.
Area Of Science
- Chronobiology
- Gerontology
- Molecular Biology
Background
- Aging is linked to physiological changes, including disrupted circadian rhythms.
- The specific mechanisms driving age-related alterations in circadian rhythms are not fully understood.
- Circulating factors in the blood may play a role in mediating these age-dependent changes.
Purpose Of The Study
- To investigate whether circulating factors in human serum mediate age-dependent changes in peripheral circadian rhythms.
- To compare the effects of serum from young and old individuals on synchronizing circadian rhythms in cultured cells.
Main Methods
- Human serum was collected from young (25-30 years) and old (70-76 years) healthy individuals.
- Serum was used to synchronize cultured fibroblasts, and reporter gene oscillations driven by clock gene promoters were measured.
- Gene expression patterns, including clock-controlled genes, were analyzed using bioinformatics tools (STRING, IPA).
Main Results
- Both young and old sera effectively initiated robust ~24-hour oscillations.
- However, young and old sera promoted cycling of distinct gene sets.
- Genes associated with oxidative phosphorylation and Alzheimer's Disease lost rhythmicity with old serum, while cholesterol biosynthesis genes increased.
- Peak expression of several clock genes (PER3, NR1D1, NR1D2, CRY1, CRY2, TEF) was delayed with old serum.
Conclusions
- Age-dependent blood-borne factors influence circadian rhythms in peripheral cells.
- These factors can impact health and disease by either maintaining or disrupting cellular rhythms.
- The study highlights a novel mechanism linking aging, circulating factors, and altered circadian gene expression patterns.
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