Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Age-related changes in gene expression in retinal microglia

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. 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

ORGANISM(S): Mus musculus

SUBMITTER: Radu Cojocaru

PROVIDER: E-GEOD-38739 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition. Microarray gene expression profiling was performed of hippocampi isolated from aged, 18 month-old Tg2576 (APPSwe-transgenic) AD mice with high Abeta plaque load relative to age-matched Tg2576 mice, which were treated for 6 months with the centrally active ACE inhibitor captopril. Another study group consisted of 12 month-old Tg2576 mice with low Abeta plaque load. In total, three study groups were analyzed, i.e. (i) 18 month-old untreated Tg2576 mice with high Abeta plaque load, (ii) age-matched Tg2576 mice treated for 6 months with the brain-penetrating ACE inhibitor captopril (20 mg/kg body weight/day in drinking water), and (iii) untreated 12 month-old Tg2576 mice with low Abeta plaque load reflecting the time point when captopril treatment was initiated. Two biological replicates were made of each group, and total hippocampal RNA of four mice was pooled for one gene chip.

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Age-related changes in gene expression in retinal microglia

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