ArticleAnnals of biomedical engineering2026
Mechanical Stretch Disrupts Calcium Dynamics and Redistributes Piezo1 in Human Astrocytes.
Article in Annals of biomedical engineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Neuroimmune Regulation in Posttraumatic Bone Repair: From Inflammatory Transition to Neurovascular Coupling and Functional Recovery.Journal of cellular physiology · 2026Review
- Neuroimmune regulation of post-traumatic bone regeneration: focus on inflammatory switching and functional recovery.Frontiers in immunology · 2026Review
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11 authors.
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Abstract
purposeAstrocytes regulate the activity of nearby neurons so disruption of astrocyte calcium dynamics by traumatic brain injury (TBI) could have profound consequences for neural network activity in the brain. This study aimed to define how mechanical stretch injury alters calcium signaling, mitochondrial membrane potential, and mechanosensitive ion channel organization in human induced pluripotent stem cell (hiPSC)-derived astrocytes.
methodsHuman iPSC-derived astrocytes were subjected to controlled two-dimensional stretch injury across multiple severities. Live-cell calcium and mitochondrial membrane potential imaging, Piezo1 immunostaining, and RNA sequencing were used to assess functional and transcriptional responses.
resultsCell viability, mitochondrial membrane potential, and spontaneous calcium transients declined in a severity-dependent manner. At moderate injury levels, reductions in mitochondrial function, calcium dynamics, and Piezo1 spatial distribution were transient. RNA sequencing identified 196 differentially expressed genes, including downregulation of mitochondrial and oxidative metabolic pathways and upregulation of cortical thinning-associated pathways.
conclusionThis platform captures functional and molecular hallmarks of astrocyte injury and provides a human in vitro model for studying mechanobiological pathways linking TBI to neurodegenerative processes.
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