Related Experiment Video
Updated: Jun 10, 2026
08:48
Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models
Published on: June 30, 2023
Changes in mitochondrial dynamics during amyloid β-induced PC12 cell apoptosis
Xiaoyu Liu1, Linqing Feng, Ming Yan
1Key Laboratory of Biomedical Engineering of Ministry of Education, Department of Biomedical Engineering, Zhejiang University, Hangzhou, Zhejiang, China.
Molecular and Cellular Biochemistry
|August 12, 2010
Summary
Alzheimer's disease (AD) involves mitochondrial changes. Amyloid beta (Aβ) exposure can cause reversible mitochondrial fragmentation in nerve cells, offering potential therapeutic targets for AD.
Area of Science:
- Neuroscience
- Cell Biology
- Mitochondrial Dynamics
Background:
- Mitochondrial dysfunction is implicated in Alzheimer's disease (AD) pathogenesis.
- Amyloid beta (Aβ) is a key factor in AD, affecting mitochondrial dynamics, but precise mechanisms remain unclear.
Purpose of the Study:
- To investigate the neurotoxicity of Aβ(25-35) on mitochondrial morphology and dynamics in PC12 cells.
- To elucidate the dynamic process of mitochondrial changes induced by Aβ(25-35) exposure.
Main Methods:
- Utilized MTT, Hoechst 33342, and Annexin V/PI assays for cell viability and apoptosis.
- Employed live cell imaging and image processing to analyze mitochondrial movement and morphology.
- Assessed mitochondrial membrane potential and reactive oxygen species (ROS) production.
Main Results:
- Aβ(25-35) exposure led to increased mitochondrial number and decreased length/size in PC12 cells, with significant changes after 6 hours.
- Short-term Aβ(25-35) exposure induced reversible mitochondrial fragmentation.
- Observed mitochondrial membrane potential dissipation, increased ROS production, and significant cell apoptosis.
Conclusions:
- Mitochondrial fission in Aβ(25-35)-induced PC12 cell apoptosis is reversible and dependent on Aβ concentration and exposure time.
- These findings suggest potential therapeutic strategies for Alzheimer's disease prevention and treatment targeting mitochondrial dynamics.
Related Concept Videos
01:45Mitochondrial Membranes
A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
01:22Cellular Injury V: Apoptosis and Autophagy
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
01:37Mitochondria
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,...