Age-related changes in gene expression in retinal microglia
Ontology highlight
ABSTRACT: In order to evaluate the gene expression profile of retinal microglia cells in different age, we purified CD11b-positive microglia from the retinas of wild type C57BL/6 mice at 3, 12, 18, and 24 months age using cell sorting method with flow cytometry. Age-related genes from isolated retinal microglia were performed using 16 Affymetrix GeneChips of Mouse Exon 1.0ST Arrays. Gene expression level between consecutive age groups (i.e. between 3 and 12 months, 12 and 18 months, and 18 and 24 months) was examined to identify microglia relevant aging genes that demonstrated significant changes. We identified a total 719 genes that showed increasing or decreasing more than 1.5-fold change (p<0.05, one-way ANOVA) for at least one of the three inter age-group comparisons. These identified genes were subjected to a hierarchical cluster analysis to visualize trends in differential expression across individual biological repeats in the 4 age groups.
Project description:In order to evaluate the gene expression profile of retinal microglia cells in different age, we purified CD11b-positive microglia from the retinas of wild type C57BL/6 mice at 3, 12, 18, and 24 months age using cell sorting method with flow cytometry. Age-related genes from isolated retinal microglia were performed using 16 Affymetrix GeneChips of Mouse Exon 1.0ST Arrays. Gene expression level between consecutive age groups (i.e. between 3 and 12 months, 12 and 18 months, and 18 and 24 months) was examined to identify microglia relevant aging genes that demonstrated significant changes. We identified a total 719 genes that showed increasing or decreasing more than 1.5-fold change (p<0.05, one-way ANOVA) for at least one of the three inter age-group comparisons. These identified genes were subjected to a hierarchical cluster analysis to visualize trends in differential expression across individual biological repeats in the 4 age groups. The microglia cells were isolated from wild type C57BL/6 mice with microglia cell specific marker CD11b conjugated with FITC using flowcytometry sorting. The aging time point was designed as 4 groups: 3 moth, 12 month, 18 month and 24 month; each group includes 4 repeats. The total RNA was extracted from isolated retinal microglia cells and reverse transcripted to cDNA after amplification and labeling. The gene expression profile was detected with Affymetrix GeneChip of Mouse Exon 1.0ST Arrays
Project description:Breast cancer is an age-related cancer in women with two peaks, one at 50 and one at 70 years of age. Here we used two conditional genetically engineered mouse models of breast cancer risk to study mammary gland transcriptional changes that occur as female mice age from 12 to 30 months of age, paralleling aging from 58 to 85 years of age in women. The two models express either mammary epithelial cell-targeted Estrogen Receptor (ER) alpha (Esr1) or Aromatase (CYP19A1A) over-expression beginning at age 12 or 18 months of age. Both of these risk factors increase estrogen pathway signaling, either directly though the receptor or by increasing local estrogen production. The goals of the study are to determine how quickly significant transcriptional changes occur in the mammary gland following transgene induction, to determine how the transcriptome becomes modified as the mice age past reproductive senescence through old and very old life stages, and to identify similarities and differences in the transcriptomes between the two risk conditions at different ages and conditions. The first specific objective of this transcriptome-based study is to identify significantly differentially expressed genes within each model between different ages and times of transgene induction. This includes transcriptional changes induced by 1 week, 6, 12 and 18 months of transgene expression with transgene expression initiated at age 12 months as well as transcriptional changes induced by 1 week and 6 months of transgene expression initiated at age 18 months. The second specific objective is to compare the two models at different ages (12, 18, 24 and 30 months of age) and different transgene induction times (6, 12 and 18 months) to identify differentially expressed genes between the models. Comparative control mice from each model include age 18- and 24-month-old mice without transgene induction.
Project description:Single-cell RNA sequencing was carried out on four selected PBMC samples of Finnish children at risk of developing Type 1 diabetes and their gender age and HLA matched control children using 10X genomic platform. All four Case children were positive for multiple islet specific autoantibodies and two of them also progressed to clinical disease during the follow up whereas the control children remain negative for all autoantibodies. Age at seroconversion for Case 2, 3, 5, and 9 children is 12, 18, 24, and 18 months, respectively. Age at sampling, in months, for the pairs was as follows (Case/Control): pair 2:24/24; pair 3: 12/18; pair 5: 12/12; pair 9:24/18.
Project description:We studied changes in gene expression in Endothelial Cells isolated from murine brains of increasing ages of 2, 6, 12, 18, and 24 months. We then performed linear regression analysis to compare the changes in gene expression in the endothelial cells with age.
Project description:Comparison of temporal small RNA gene expression profiles from Danio rerio skin. The smallRNA-seq data comprise 5 age groups at 6, 12, 24, 36 and 42 months. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Project description:Comparison of temporal small RNA gene expression profiles from Danio rerio brain. The smallRNA-seq data comprise 5 age groups at 6, 12, 24, 36 and 42 months. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Project description:C57Bl6/J female mice were ovariectomized or not at the age of 12 months and then euthanized 12 months later at the age of 24 months. Half of the females received for 28 days an angiotensin II (AngII; 1.5 mg/kg/day) continuous infusion starting at the age of 23 months. The mice were provided with a running wheel during the 12 months after gonadectomy with the exception of the last month before euthanasia.
Project description:Whole body knockout mice lacking IQ-motif containing GTPase-activating protein 2 (IQGAP2) develop spontaneous hepatocellular carcinoma (HCC) at the age of 12 months and older (Schmidt et al., 2008). Hepatic transcript expression profiles were obtained for IQGAP2 knockout and wild-type control mice of two age groups, 6- and 24-month-old. Liver samples from 24-month-old IQGAP2 knockout mice were HCC tumors, livers from all other groups were tumor-free. Results provide insights into the potential role of IQGAP2 as a liver-specific tumor suppressor.
Project description:C57Bl6/J male and female mice were gonadectomized or not at the age of 12 months and then euthanized 12 months later at the age of 24 months. Half of the females received for 28 days an angiotensin II (AngII; 1.5 mg/kg/day) continuous infusion starting at the age of 23 months. The mice were provided with a running wheel during the 12 months after gonadectomy with the exception of the last month before euthanasia.
Project description:Background: The prognostic impact of segmental chromosome alterations (SCAs) in children older than 1 year, diagnosed with localised unresectable neuroblastoma (NB) without MYCN amplification enrolled in the European Unresectable Neuroblastoma (EUNB) protocol is still to be clarified, while, for other group of patients, the presence of SCAs is associated with poor prognosis. Methods: To understand the role of SCAs we performed multilocus/pangenomic analysis of 98 tumour samples from patients enrolled in the EUNB protocol. Results: Age at diagnosis was categorised into two groups using 18 months as the age cutoff. Significant difference in thepresence of SCAs was seen in tumours of patients between 12 and 18 months and over 18 months of age at diagnosis, respectively (P<0.04). A significant correlation (P<0.03) was observed between number of SCAs per tumour and age. Event-free (EFS) andoverall survival (OS) were calculated in both age groups, according to both the presence and number of SCAs. In older patients, a poorer survival was associated with the presence of SCAs (EFS<46% vs 75%, P<0.023; OS<66.8% vs 100%, P<0.003). Moreover, OS of older patients inversely correlated with number of SCAs (P<0.002). Finally, SCAs provided additional prognostic information beyond histoprognosis, as their presence was associated with poorer OS in patients over 18 months with unfavourable International Neuroblastoma Pathology Classification (INPC) histopathology (P<0.018). Conclusions: The presence of SCAs is a negative prognostic marker that impairs outcome of patients over the age of 18 months with localised unresectable NB without MYCN amplification, especially when more than one SCA is present. Moreover, in older patients with unfavourable INPC tumour histoprognosis, the presence of SCAs significantly affects OS.