Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

12.7K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
12.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Reduced LACTB expression in myeloid cells is associated with elevated succinylcarnitine levels and reduced Alzheimers disease risk.

bioRxiv : the preprint server for biology·2026
Same author

Epigenetic control of microglial developmental milestones from proliferative progenitors to efficient phagocytes.

Research square·2026
Same author

Treatment resistance to platinum-based chemotherapy in lung and ovarian cancer is driven by a targetable TGFβ senescent secretome.

Nature aging·2026
Same author

A Hundred Years of the Chemosensory Synapse: A Tribute to Fernando de Castro.

Acta physiologica (Oxford, England)·2025
Same author

Phosphodiesterase Inhibition Increases Striatal GDNF and Protects Against Preclinical Parkinsonism.

Journal of neurochemistry·2025
Same author

Epigenetic control of microglial developmental milestones from proliferative progenitors to efficient phagocytes.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Jun 19, 2025

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
10:20

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

39.6K

Microglia mitochondrial complex I deficiency during development induces glial dysfunction and early lethality.

Bella Mora-Romero1,2,3, Nicolas Capelo-Carrasco1,3,4, Juan J Pérez-Moreno5,6,7

  • 1Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, Spain.

Nature Metabolism
|July 24, 2024
PubMed
Summary

Mitochondrial defects in microglia contribute to primary mitochondrial diseases (PMDs). Impaired Complex I in these brain immune cells causes dysfunction and neurological symptoms, suggesting a novel therapeutic target for PMDs.

More Related Videos

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

15.8K
Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
10:21

Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation

Published on: February 16, 2018

19.3K

Related Experiment Videos

Last Updated: Jun 19, 2025

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
10:20

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

39.6K
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

15.8K
Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
10:21

Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation

Published on: February 16, 2018

19.3K

Area of Science:

  • Neuroscience
  • Immunology
  • Mitochondrial Biology

Background:

  • Primary mitochondrial diseases (PMDs) often involve neurological disorders linked to oxidative phosphorylation (OXPHOS) defects.
  • Gliosis and symptom amelioration via microglial depletion in PMD models suggest a role for these brain immune cells.

Purpose of the Study:

  • To investigate if OXPHOS deficits specifically in microglia contribute to the pathology of PMDs.
  • To understand the role of mitochondrial Complex I (CI) in microglial function and its impact on neurological health.

Main Methods:

  • In vitro studies assessing microglial metabolic response to stimulation and CI inhibition (rotenone).
  • Generation and analysis of a mouse model with CI deficiency specifically in microglia (MGcCI).
  • Assessment of microglial morphology, gene expression, brain pathology (gliosis, synaptic markers), and behavioral deficits in MGcCI mice.

Main Results:

  • Microglial stimulation showed altered metabolic rewiring with CI inhibition in vitro.
  • MGcCI mice exhibited microglial metabolic and transcriptional changes, leading to hypertrophy and dysfunction.
  • MGcCI mice displayed reactive astrocytes, synaptic loss, altered neuronal populations, behavioral deficits, and premature death, partially rescued by microglial depletion.

Conclusions:

  • Microglial development and function are dependent on mitochondrial Complex I activity.
  • OXPHOS deficits in microglia represent a direct contribution to primary mitochondrial diseases, offering new therapeutic avenues.