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.

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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.

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Study IDST003249
Study TitleMitochondrial respiration impairment in microglia dampens response to demyelinating injury but is not sufficient to induce an aging phenotype
Study SummaryMicroglia 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 NameStoolman
First NameJoshua
Address303 E Superior Street,
Emailjoshua.stoolman@northwestern.edu
Phone7343559440
Submit Date2024-01-19
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2024-06-11
Release Version1
Joshua Stoolman Joshua Stoolman
https://dx.doi.org/10.21228/M8WJ8H
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Genotype Sample source
SA353485Nav-Jos-20220209-02HET Microglia
SA353486Nav-Jos-20220209-04HET Microglia
SA353487Nav-Jos-20220209-07HET Microglia
SA353488Nav-Jos-20220209-09HET Microglia
SA353489Nav-Jos-20220209-19HET Microglia
SA353490Nav-Jos-20220209-22HET Microglia
SA353491Nav-Jos-20220209-03KO Microglia
SA353492Nav-Jos-20220209-05KO Microglia
SA353493Nav-Jos-20220209-08KO Microglia
SA353494Nav-Jos-20220209-10KO Microglia
SA353495Nav-Jos-20220209-20KO Microglia
SA353496Nav-Jos-20220209-21KO Microglia
SA353497Nav-Jos-20220209-01N/A Plasma
SA353498Nav-Jos-20220209-06N/A Plasma
SA353499Nav-Jos-20220209-16N/A Plasma
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