Summary of Study ST003249
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002017. The data can be accessed directly via it's Project DOI: 10.21228/M8WJ8H This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
Study ID | ST003249 |
Study Title | Mitochondrial respiration impairment in microglia dampens response to demyelinating injury but is not sufficient to induce an aging phenotype |
Study Summary | Microglia are necessary for CNS function during development and play roles in aging, Alzheimer’s Disease (AD) and the response to demyelinating injury1–5. Mitochondrial respiratory chain (RC) controls macrophage-dependent immune responses6–9. However, whether mitochondrial RC is essential to microglia function is not known. We conditionally deleted the mitochondrial complex III subunit Rieske Iron-Sulfur Protein (RISP) in the microglia of adult mice to assess the requirement of microglial RC for survival, proliferation, and adult CNS function in vivo. Surprisingly, mitochondrial RC function was not required for survival or proliferation of microglia in vivo. RNA-seq analysis showed that loss of RC function in microglia caused changes in gene expression distinct from aged or disease-associated microglia (DAM). Microglia-specific loss of mitochondrial RC function did not affect cognitive decline during aging or in the 5xFAD model of Alzheimer’s disease (AD). However, Abeta plaque coverage decreased and microglial interaction with Abeta plaques increased in the hippocampus of 5xFAD mice with mitochondrial RC-deficient microglia. Microglia-specific loss of mitochondrial RC function did impair remyelination following an acute, reversible demyelinating event. Thus, mitochondrial respiration in microglia is dispensable for maintenance of normal cognitive function but is essential to maintain a proper response to CNS demyelinating injury. |
Institute | Northwestern University |
Last Name | Stoolman |
First Name | Joshua |
Address | 303 E Superior Street, |
joshua.stoolman@northwestern.edu | |
Phone | 7343559440 |
Submit Date | 2024-01-19 |
Raw Data Available | Yes |
Raw Data File Type(s) | raw(Thermo) |
Analysis Type Detail | LC-MS |
Release Date | 2024-06-11 |
Release Version | 1 |
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Subject:
Subject ID: | SU003368 |
Subject Type: | Mammal |
Subject Species: | Mus musculus |
Taxonomy ID: | 10090 |
Age Or Age Range: | 1 year |
Gender: | Male and female |