Summary of project PR002017
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
| Project ID: | PR002017 |
| Project DOI: | doi: 10.21228/M8WJ8H |
| Project Title: | Mitochondrial respiration in microglia is essential for response to demyelinating injury but not proliferation. |
| Project Summary: | Microglia are necessary for CNS function during development and play roles in aging, Alzheimer’s Disease (AD) and the response to demyelinating injury. Mitochondrial respiratory chain (RC) controls macrophage-dependent immune responses. 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 Feinberg School of Medicine |
| Last Name: | Stoolman |
| First Name: | Joshua |
| Address: | 303 E Superior Street, |
| Email: | joshua.stoolman@northwestern.edu |
| Phone: | 7343559440 |
Summary of all studies in project PR002017
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST003249 | Mitochondrial respiration impairment in microglia dampens response to demyelinating injury but is not sufficient to induce an aging phenotype | Mus musculus | Northwestern University | MS | 2024-06-11 | 1 | 15 | Uploaded data (1.2G)* |
