Astrocytic Responses to Injury by Laser-Induced Shockwave
<p dir="ltr">Astrocytes play a key role in supporting neuronal survival and recovery following brain injury. Traumatic brain injury (TBI), particularly blast-induced TBI (bTBI), leads to significant neuronal death, where calcium dysregulation is a critical secondary consequence. This...
محفوظ في:
| المؤلف الرئيسي: | |
|---|---|
| مؤلفون آخرون: | , , , , |
| منشور في: |
2025
|
| الموضوعات: | |
| الوسوم: |
إضافة وسم
لا توجد وسوم, كن أول من يضع وسما على هذه التسجيلة!
|
| الملخص: | <p dir="ltr">Astrocytes play a key role in supporting neuronal survival and recovery following brain injury. Traumatic brain injury (TBI), particularly blast-induced TBI (bTBI), leads to significant neuronal death, where calcium dysregulation is a critical secondary consequence. This study employed laser-induced shockwave (LIS) to model blast injury and investigate astrocytic calcium signaling responses in both wild-type (WT) and Alzheimer’s disease (AD)-related cells.</p><p dir="ltr">Astrocytes were calcium-stained and exposed to LIS, followed by 30 minutes of time-lapse imaging. Live and dead cells were differentiated using Fluo4-AM and HCred filters. ImageJ, MATLAB, and subsequent statistical analysis were used to quantify calcium intensity changes, peak rise rates, and spatial dynamics within cells.</p><p dir="ltr">Results revealed that AD astrocytes exhibited significantly greater calcium increases compared to WT astrocytes. Moreover, calcium elevation was higher in AD nuclei than in their cytoplasm, indicating compartment-specific dysregulation. The peak rise rate in AD nuclei and cytoplasm was approximately 3 s⁻¹ greater than that observed in WT counterparts. These findings highlight a marked impairment in calcium regulation in AD astrocytes following injury.</p><p dir="ltr">The observed dysregulation is clinically relevant, as impaired calcium handling contributes to secondary neuronal death and may accelerate neurodegenerative processes underlying Alzheimer’s disease. Expanding this study with larger sample sizes will help clarify the molecular pathways linking astrocytic calcium imbalance to neuronal vulnerability.</p><p dir="ltr">This work advances understanding of astrocytic responses to injury and supports further exploration of calcium regulation as a therapeutic target for brain trauma and neurodegeneration.</p> |
|---|