Project description:To uncover abnormally regulated genes in OGT-KO SCs, we performed gene expression profiling experiments using sciatic nerves from 1-month-old OGT-SCKO and wildtype mice.
Project description:Sciatic nerve ligation was performed on cohorts of 2-month and 24-month old animals. Resulting gene-expression data were generated from sciatic nerve 1 and 4 days after injury compared to naïve animals. Results show differences in sciatic nerve responses with normal aging. Total RNA taken from sciatic nerves from 2-month and 24-month old animals at either day 0, 1 and 4 after sciatic nerve crush injury.
Project description:Gene expression analysis of 2-month-old Ctrl and Tfam-SCKO mice. At this age mitochondrial function is disrupted in the Schwann cells of Tfam-SCKO mice ,but their nerves display only very limited pathology. Mitochondrial dysfunction is a common cause of peripheral neuropathy. Much effort has been devoted to examining the role played by neuronal/axonal mitochondria, but how mitochondrial deficits in peripheral nerve glia (Schwann cells, SCs) contribute to peripheral nerve diseases remains unclear. Here, we investigate a mouse model of peripheral neuropathy secondary to SC mitochondrial dysfunction (Tfam-SCKOs). We show that disruption of SC mitochondria activates a maladaptive integrated stress response through actions of heme-regulated inhibitor kinase (HRI), and causes a shift in lipid metabolism away from fatty acid synthesis toward oxidation. These alterations in SC lipid metabolism result in depletion of important myelin lipid components as well as in accumulation of acylcarnitines, an intermediate of fatty acid b-oxidation. Importantly, we show that acylcarnitines are released from SCs and induce axonal degeneration. A maladaptive integrated stress response as well as altered SC lipid metabolism are thus underlying pathological mechanisms in mitochondria-related peripheral neuropathies. Total RNA samples were prepared by isolating and pooling RNA from three different 2-month-old MPZ-Tfam KO and Ctrl mice. 2 replicates per genotype were used in this experiment and they were prepared entirely independently.
Project description:Transcription profiling of heart ventricles from 10 week old mice heterozygous for dn-p21ras and 3 month old wild type FVB mice to study severe dilated cardiomyopathy.
Project description:Transcriptomics and phosphoproteomics were carried out in B6.Cg-Mapttm1(EGFP)Klt (mapt knockout: tau-KO) and wild-type (WT) 12-month-old mice to learn about the effects of tau ablation.
Project description:Sciatic nerve ligation was performed on cohorts of 2-month and 24-month old animals. Resulting gene-expression data were generated from sciatic nerve 1 and 4 days after injury compared to naïve animals. Results show differences in sciatic nerve responses with normal aging.
Project description:The objective of this study was to determine which pathways are significantly regulated with age in sciatic and radial nerves, individually or considering the interaction term. We find a strong signature of the cholesterol biosynthesis pathway being downregulated with age in both nerves, however, this effect is significantly milder in the radial nerve. We collected both radial and sciatic nerves from 8 adult (8 months old) and 8 old (24 months old) rats.
Project description:Transcription profiling by array of mouse CD8 central memory T-cells derived from spleens of 7-month old PD-1 knockout or wild-type mice
Project description:In order to uncover the biological processes affected in glial cells by aging, we analyzed microarray gene expression of the Schwann cell-rich mouse sciatic nerve at 17 time-points throughout life, from day of birth until senescence. In addition, we combined these data with the microarray gene expression data of myelin 56 day-old mouse mutants carrying deletions of either Pmp22, SCAP or Lpin1. Seven mice were dissected per developmental or aging time-point. Both sciatic nerves were isolated from each mouse and tissues were pooled per time-point to extract total RNA. For the mutants and their wild-type littermates, sciatic nerves were dissected from three mice per genotype. Tissues were not pooled, which generated triplicates per genotype. Total RNA was extracted, purified and quality-controlled. For each condition, 300 ng of total RNA was used to synthesize cRNA using the Illumina TotalPrep RNA amplification kit (Ambion). The cRNA was then quantified, quality controlled and hybridized to the MouseWG-6 v1 expression Beadchips (Illumina) according to the manufacturerM-^Rs instructions.
