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Updated: Feb 7, 2026
12:48
Measuring Near Plasma Membrane and Global Intracellular Calcium Dynamics in Astrocytes
Published on: April 26, 2009
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Mechanical Stretch Disrupts Calcium Dynamics and Redistributes Piezo1 in Human Astrocytes
Shahrzad Shiravi1, Akash Chakka2, Xi Xiao2
1Department of Mechanical and Industrial Engineering, University of Illinois Chicago, Chicago, IL, 60607, USA.
Annals of Biomedical Engineering
|February 5, 2026
Summary
Traumatic brain injury (TBI) disrupts astrocyte calcium signaling and mitochondrial function. This study models TBI in human astrocytes, revealing severity-dependent functional declines and identifying key molecular pathways involved in neurodegeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Biomedical Engineering
Background:
- Astrocytes play a crucial role in regulating neuronal activity.
- Disruption of astrocyte calcium dynamics by traumatic brain injury (TBI) can significantly impact neural network function.
- Understanding astrocyte responses to mechanical injury is vital for comprehending TBI pathogenesis.
Purpose of the Study:
- To investigate the effects of mechanical stretch injury on calcium signaling, mitochondrial membrane potential, and mechanosensitive ion channel organization in human induced pluripotent stem cell (hiPSC)-derived astrocytes.
- To establish a human in vitro model for studying the mechanobiology of TBI.
Main Methods:
- Human iPSC-derived astrocytes were subjected to controlled two-dimensional stretch injury.
- Live-cell imaging was used to assess calcium dynamics and mitochondrial membrane potential.
- Piezo1 immunostaining and RNA sequencing were employed to analyze molecular and cellular responses.
Main Results:
- Cell viability, mitochondrial membrane potential, and spontaneous calcium transients decreased with increasing injury severity.
- Moderate injury caused transient reductions in mitochondrial function, calcium dynamics, and Piezo1 distribution.
- RNA sequencing revealed differential expression of 196 genes, including altered mitochondrial/metabolic and cortical thinning-associated pathways.
Conclusions:
- The developed platform effectively captures functional and molecular aspects of astrocyte injury.
- This human in vitro model provides a valuable tool for investigating the mechanobiological pathways linking TBI to neurodegenerative diseases.
- Findings highlight the complex cellular responses of astrocytes to mechanical forces relevant to TBI.
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