Project description:We report the global gene expression in follicular (FO) B cells and age/autoimmunity-associated B cells (ABCs). We found that Fc-receptor like (Fcrl) 5 was highly expressed in ABCs isolated from 50-week-old mice, compared to FO B cells. This study provides a basis for understanding the relationship between autoimmune diseases and Fcrl5 expression in B cells.
Project description:The origin and nature of recently discovered age-associated B cells (ABCs) is under investigation. We used a microarray to examine the transcriptional signatures of ABCs, follicular B cells from aged mice (AFO), and follicular B cells from young mice (YFO).
Project description:Hippocampal tissues from young and middle-aged C57BL/6J mice were harvested at 4-hour intervals over two days and processed for proteomic analysis using label-free quantification.
Project description:Mice deficient in the glucocorticoid-regenerating enzyme 11β-HSD1 resist age-related spatial memory impairment. To investigate the mechanisms/pathways involved, we used microarrays to identify differentially expressed hippocampal genes that associate with cognitive ageing and 11β-HSD1. Aged wild-type mice were separated into memory-impaired and unimpaired relative to young controls according to their performance in the Y-maze. All individual aged 11β-HSD1-deficient mice showed intact spatial memory. The majority of differentially expressed hippocampal genes were increased with ageing (e.g. immune/inflammatory response genes) with no genotype differences. However, the neuronal-specific transcription factor, Npas4 and immediate early gene, Arc were reduced (relative to young) in the hippocampus of memory-impaired but not unimpaired aged wild-type or aged 11β-HSD1-deficient mice. Quantitative RT-PCR and in situ hybridization confirmed reduced Npas4 and Arc mRNA expression in memory-impaired aged wild-type mice. These findings suggest that 11β-HSD1 may contribute to the decline in Npas4 and Arc mRNA levels associated with memory impairment during ageing, and that decreased activity of synaptic plasticity pathways involving Npas4 and Arc may, in part, underlie the memory deficits seen in cognitively-impaired aged wild-type mice. 20 samples, 5 groups of 4 biological replicates each. Young, Wild Type animals are overall controls
Project description:Analysis of function of CD11c+ cells from middle-aged and young mice at gene level. This experiment provided insight into the different genes that plays roles in inflammation, immune response and mainly arachidonic acid cascade that are differentiall expressed in CD11c+ cells from middle aged and young mice. Total RNA was isolated from pulmonary CD11c cells (separated using magnetic beads) from middle-aged and young mice
Project description:T cells change substantially with age and are involved in atherosclerosis. Aging is the strongest clinical risk factor for atherosclerosis so we profiled T cells in young and aged mice prior to atherosclerosis (healthy) and in young and aged atherosclerotic mice (diseased).
Project description:Mice deficient in the glucocorticoid-regenerating enzyme 11β-HSD1 resist age-related spatial memory impairment. To investigate the mechanisms/pathways involved, we used microarrays to identify differentially expressed hippocampal genes that associate with cognitive ageing and 11β-HSD1. Aged wild-type mice were separated into memory-impaired and unimpaired relative to young controls according to their performance in the Y-maze. All individual aged 11β-HSD1-deficient mice showed intact spatial memory. The majority of differentially expressed hippocampal genes were increased with ageing (e.g. immune/inflammatory response genes) with no genotype differences. However, the neuronal-specific transcription factor, Npas4 and immediate early gene, Arc were reduced (relative to young) in the hippocampus of memory-impaired but not unimpaired aged wild-type or aged 11β-HSD1-deficient mice. Quantitative RT-PCR and in situ hybridization confirmed reduced Npas4 and Arc mRNA expression in memory-impaired aged wild-type mice. These findings suggest that 11β-HSD1 may contribute to the decline in Npas4 and Arc mRNA levels associated with memory impairment during ageing, and that decreased activity of synaptic plasticity pathways involving Npas4 and Arc may, in part, underlie the memory deficits seen in cognitively-impaired aged wild-type mice.