Project description:The impact of aging on intestinal stem cells (ISCs) has not been fully elucidated. In this study, we identified widespread epigenetic and transcriptional alterations in old ISCs. Using a reprogramming algorithm, we identified a set of key transcription factors (Egr1, Irf1, FosB) that drives molecular and functional differences between old and young states. Overall, by dissecting the molecular signature of aged ISCs, our study identified transcription factors that enhance the regenerative capacity of ISCs.
Project description:To explore the effects of gut microbiota of young (8 weeks) or old mice (18~20 months) on stroke, feces of young (Y1-Y9) and old mice (O6-O16) were collected and analyzed by 16s rRNA sequencing. Then stroke model was established on young mouse receive feces from old mouse (DOT1-15) and young mouse receive feces from young mouse (DYT1-15). 16s rRNA sequencing were also performed for those young mice received feces from young and old mice.
Project description:The impact of aging on intestinal stem cells (ISCs) has not been fully elucidated. In this study, we identified widespread epigenetic and transcriptional alterations in old ISCs. Using a reprogramming algorithm, we identified a set of key transcription factors (Egr1, Irf1, FosB) that drives molecular and functional differences between old and young states. Overall, by dissecting the molecular signature of aged ISCs, our study identified transcription factors that enhance the regenerative capacity of ISCs.
Project description:The impact of aging on intestinal stem cells (ISCs) has not been fully elucidated. In this study, we identified widespread epigenetic and transcriptional alterations in old ISCs. Using a reprogramming algorithm, we identified a set of key transcription factors (Egr1, Irf1, FosB) that drives molecular and functional differences between old and young states. Overall, by dissecting the molecular signature of aged ISCs, our study identified transcription factors that enhance the regenerative capacity of ISCs.
Project description:To examine underlying differences in gene expression between young and old MSCs and the effects of exposure of old MSCs to media conditioned by young MSCs on gene expression we performed RNA sequencing
Project description:<p>The roles of specific microbial metabolites in aging remains understudied. Here we examine the microbiome’s contribution to the metabolic profile in aged mice. Fecal samples were collected from 8-week-old (young) and 18-month-old (aged) female Swiss-Webster mice raised conventionally (Conv) or germ free (GF). Bacterial DNA was sequenced and microbiome analysis predormed using QIIME2. Liquid chromatography mass spectrometry was used for untargeted metabolomics on Conv and GF samples.</p><p>Significant differences were observed in bacterial composition and predicted functional pathways between young and aged mice. Age-related metabolome variance was greater in Conv than GF mice, highlighting microbial contribution. Moreover, microbiome-associated metabolites, predominantly lipids, were higher in aged mice, with linoleic acid metabolism enriched in this group. Our study underscores a microbiome-dependent component to age-related metabolic changes, particularly in lipid-associated pathways. These findings contribute to the growing body of literature linking gut microbiota with host metabolism in aging.</p>
Project description:Anabolic activities such as ribosome biogenesis and protein synthesis are linked to aging. Ribosomal RNA (rRNA) synthesis is the limiting step of ribosome biogenesis, thus dictating the number of ribosomes in cells and, consequently, the capacity for mRNA translation. Knockdown of the rRNA synthesis repressor, NCL-1, accelerated aging, whereas knocking down the transcription initiation factor C36E8.1 promoted longevity. This suggested that rRNA synthesis has a negative correlation with lifespan. To investigate the metabolic changes upon manipulation of rRNA synthesis the proteome of NCL-1 KD and C36E8.1 KD were analyzed at young, middle, and old age (AD2, AD6, AD12).