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Suppressed cellular senescence mediated by T-box3 in aged gastric epithelial cells may contribute to aging-related carcinogenesis

ABSTRACT: Aging is a risk factor of carcinogenesis in various organs, and abnormal aging of the stem cells is considered responsible for carcinogenesis. Recent advances in organoid culturing system have made it viable to investigate mini organs developed from tissue stem cells. In this study, we aimed to investigate the implications of aging stem cells for gastric carcinogenesis. We found that gastric organoids of aged mice grew larger in size and proliferated vigorously compared to that of young mice. To elucidate the mechanism involved in this difference, we extracted the total RNA from the organoids and subjected it to microarray analysis, which revealed that the expression of transcription factor T-box 3 (Tbx3) was enhanced in aged gastric organoids. Further studies showed that this enhanced Tbx3 expression suppressed cellular senescence and enhanced proliferation. We utilized microarray analysis to find out the gene responsible for restraining cellular senescence in aged gastric organoids.

ORGANISM(S): Mus musculus

PROVIDER: GSE185680 | GEO | 2023/03/22

REPOSITORIES: GEO

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Project description:A detailed knowledge of the mechanisms underlying brain aging is fundamental to understand its functional decline and the baseline upon which brain pathologies superimpose. Endogenous protective mechanisms must contribute to the adaptability and plasticity still present in the healthy aged brain. Apolipoprotein D (ApoD) is one of the few genes with a consistent and evolutionarily conserved up-regulation in the aged brain. ApoD protecting roles upon stress or injury are well known, but a study of the effects of ApoD expression in the normal aging process is still missing. Using an ApoD-knockout mouse we analyze the effects of ApoD on factors contributing to the functional maintenance of the aged brain. We focused our cellular and molecular analyses in cortex and hippocampus at an age representing the onset of senescence where mortality risks are below 25%, avoiding bias towards long-lived animals. Lack of ApoD causes a prematurely aged brain without altering lifespan. Age-dependent hyperkinesia and memory deficits are accompanied by differential molecular effects in cortex and hippocampus. Transcriptome analyses reveal distinct effects of ApoD loss on the molecular age-dependent patterns of cortex and hippocampus, with different cell-type contributions to age-regulated gene expression. Markers of glial reactivity, proteostasis, and oxidative and inflammatory damage reveal early signs of aging and enhanced brain deterioration in the ApoD-knockout brain. The lack of ApoD results in an age-enhanced significant reduction in neuronal calcium-dependent functionality markers and signs of early reduction of neuronal numbers in the cortex, thus impinging upon parameters clearly differentiating neurodegenerative conditions from healthy brain aging. Our data support the hypothesis that the physiological increased brain expression of ApoD represents a homeostatic anti-aging mechanism. The brain cortex and hippocampus of young and aged mice of wild-type and ApoD-KO genotypes were used for RNA extraction and hybridization on Affymetrix microarrays. We aim at identifying distinct effects of ApoD loss on the molecular age-dependent patterns of cortex and hippocampus.

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Suppressed cellular senescence mediated by T-box3 in aged gastric epithelial cells may contribute to aging-related carcinogenesis

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