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Mitochondria

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

Translocation of Proteins into the Mitochondria

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...

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Related Experiment Video

Updated: Jul 30, 2025

Author Spotlight: Decoding Mitochondrial Aging

Author Spotlight: Decoding Mitochondrial Aging

Published on: June 30, 2023

APOE expression and secretion are modulated by mitochondrial dysfunction.

Meghan E Wynne¹, Oluwaseun Ogunbona^1,2, Alicia R Lane¹

¹Department of Cell Biology, Emory University, Atlanta, United States.

|May 12, 2023

Summary

This summary is machine-generated.

Mitochondria regulate cellular secrets, including Alzheimer's disease risk factor apolipoprotein E (APOE). Disrupting mitochondrial electron transport chain upregulates APOE, suggesting mitochondria are key upstream regulators in health and disease.

Keywords:

APOE alzheimer's disease cell biology human mitochondria neuroscience

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Area of Science:

Cellular Biology
Neuroscience
Mitochondrial Biology

Background:

Mitochondria are crucial for cellular function, impacting processes via cell-autonomous and non-cell-autonomous mechanisms.
Mitochondrial regulation of the secretome, including secreted factors, is increasingly recognized for its role in cellular communication.

Purpose of the Study:

To investigate the role of mitochondrial electron transport chain (ETC) function in regulating the cellular secretome.
To determine if ETC disruption influences the expression and secretion of Alzheimer's disease risk factors like apolipoprotein E (APOE).

Main Methods:

Genetic and pharmacological disruption of mitochondrial ETC complexes (I, III, IV) and SLC25A transporters.
Analysis of APOE transcript, protein levels, and secretion in various cell types, including iPSC-derived human astrocytes.
In vivo studies using the 5xFAD mouse model to assess age- and genotype-dependent changes in mitochondrial complex I and APOE levels.

Main Results:

Disruption of the ETC, directly or indirectly, led to a significant upregulation (up to 49-fold) of APOE transcript, protein, and secretion.
APOE upregulation was observed across diverse cell types and in human astrocytes, indicating an inflammatory gene expression program.
In the 5xFAD mouse model, a decline in respiratory complex I preceded an increase in brain APOE levels.

Conclusions:

Mitochondria act as novel upstream regulators of APOE, influencing its expression and secretion.
Mitochondrial dysfunction may contribute to APOE-related cellular processes in both health and disease, particularly in neurodegenerative conditions like Alzheimer's disease.