Expression data from 10 months old sciatic nerves of Sterol regulatory element binding factor 1c (SREBF-1c) KO mice and relative littermates
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE65754 | GEO | 2015/02/10
SECONDARY ACCESSION(S): PRJNA274955
REPOSITORIES: GEO
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Project description:SREBF-1c is a transcription factor regulating fatty acid biosynthesis. We have charaterized the impact of the abcence of SREBF-1c on the development of peripheral neuropathy In this dataset we included expression data from dissected sciatic nerve from 10 months old SREBF-1c KO mice and relative littermates. 6 total samples were analyzed (3 wild type and 3 SREBF-1c KO). Data handling was mainly done using TAC and Partek Genomic Suite software. The Robust Multichip Average (RMA) method was employed to calculate probe set intensity. RMA is a robust multi-chip average expression method that estimates the probe-level data from a set of chips: the perfect-match (PM) values are background-corrected, normalized and finally summarized resulting in a set of expression measures. The identification of differentially expressed genes was addressed using Fold Change (FC) and ANOVA. For each experimental condition the probesets whose fold change are higher or equal than 1.5 with an ANOVA unadjusted p-value lower than 0,05 are selected as significantly modulated.
2015-02-10 | E-GEOD-65754 | biostudies-arrayexpress
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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.
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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.
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