Gene expression profiles of p16high and p16low adipocyte progenitor cells in the gonadal adipose tissue of 18 month old mice [scRNA_Adipose]
Ontology highlight
ABSTRACT: We used scRNA-seq analysis to investigate the expression profiles of p16high adipocyte progenitor cells compared with p16low adipocyte progenitor cells in the gonadal adipose tissue of aging mice.
Project description:We used bulk RNA-seq analysis to investigate the gene expression patterns of p16high adipocyte progenitor cells compared with p16low adipocyte progenitor cells in the gonadal adipose tissue of tumor bearing mice.
Project description:Gene expression profiles of p16high and p16low adipocyte progenitor cells in the gonadal adipose tissue of 18 month old mice [scRNA_Adipose]
Project description:Gene expession profiles of p16high and p16low adipocyte progenitor cells of gonadal adipose tissue in the cancer cachexia mouse model
Project description:To determine the transcriptomic effects of LAMA4 loss on adipose tissue structure and gene expression in two dietary paradigms, we assessed gonadal white adipose tissue of male control and adipocyte-specific LAMA4 knockout mice using a Quant-Seq strategy.
Project description:The accumulation of senescent cells can drive many age-associated phenotypes and pathologies. Consequently, it has been proposed that removing senescent cells might extend lifespan. Here we generated two knock-in mouse models targeting the best-characterized marker of senescence, p16Ink4a. Using a genetic lineage tracing approach, we found that age-induced p16High senescence is a slow process that manifests around 10-12 months of age. The majority of p16High cells were vascular endothelial cells mostly in liver sinusoids (LSECs), and to lesser extent macrophages and adipocytes. In turn, continuous or acute elimination of p16High senescent cells disrupted blood–tissue barriers with subsequent liver and peri-vascular tissue fibrosis and health deterioration. Our data show that senescent LSECs are not replaced after removal and have important structural and functional roles in the aging organism. In turn, delaying senescence or replacement of senescent LSECs could represent a powerful tool in slowing down aging.
Project description:We used scRNA-seq analysis to investigate the characteristics and communication of p16high cancer stromal cells in the tumor microenvironment.
Project description:Multiple mechanisms and pathophysiological changes after anesthesia, such as brain aging and neurodegenerative diseases. And the gene transcription patterns and modulation networks after general anesthesia remains to be elucidated. We used microarrays to detail the global programme of gene expression in rats after sevoflurane anesthesia and identified distinct classes of changed.