ArticleScientific reports2016
Blast shockwaves propagate Ca(2+) activity via purinergic astrocyte networks in human central nervous system cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Repetitive Low-Level Blast Exposure Alters Circulating Myeloperoxidase, Matrix Metalloproteinases, and Neurovascular Endothelial Molecules in Experienced Military Breachers.International journal of molecular sciences · 2025Article
- Exploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Advancing next-generation brain organoid platforms for investigating traumatic brain injury from repeated blast exposures.Frontiers in bioengineering and biotechnology · 2025Review
- Astrocytes sense glymphatic-level shear stress through the interaction of sphingosine-1-phosphate with Piezo1.iScience · 2024Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
- Chronic intermittent ethanol exposure disrupts stress-related tripartite communication to impact affect-related behavioral selection in male rats.Neurobiology of stress · 2023Article
- The Imbalance of Astrocytic Mitochondrial Dynamics Following Blast-Induced Traumatic Brain Injury.Biomedicines · 2023Article
- Models of traumatic brain injury-highlights and drawbacks.Frontiers in neurology · 2023Review
- A single cell death is disruptive to spontaneous CaFrontiers in cellular neuroscience · 2022Article
- Analyzing pericytes under mild traumatic brain injury using 3D cultures and dielectric elastomer actuators.Frontiers in neuroscience · 2022Article
- Blast-induced temporal alterations in blood-brain barrier properties in a rodent model.Scientific reports · 2021Article
- Laser-Induced Shockwave (LIS) to Study Neuronal CaFrontiers in bioengineering and biotechnology · 2021Article
- Response to Blast-like Shear Stresses Associated with Mild Blast-Induced Brain Injury.Biophysical journal · 2019Article
- Multispectral imaging of cortical vascular and hemodynamic responses to a shock wave: observation of spreading depolarization and oxygen supply-demand mismatch.Journal of biomedical optics · 2019Article
- Low-energy shock waves evoke intracellular CaScientific reports · 2019Article
- Proteomics Analysis Reveals the Implications of Cytoskeleton and Mitochondria in the Response of the Rat Brain to Starvation.Nutrients · 2019Article
- Astrocyte Mechano-Activation by High-Rate Overpressure Involves Alterations in Structural and Junctional Proteins.Frontiers in neurology · 2019Article
- Mild Blast Injury Produces Acute Changes in Basal Intracellular Calcium Levels and Activity Patterns in Mouse Hippocampal Neurons.Journal of neurotrauma · 2018Article
- Astroglial CaFrontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
In a recent study of the pathophysiology of mild, blast-induced traumatic brain injury (bTBI) the exposure of dissociated, central nervous system (CNS) cells to simulated blast resulted in propagating waves of elevated intracellular Ca(2+). Here we show, in dissociated human CNS cultures, that these calcium waves primarily propagate through astrocyte-dependent, purinergic signaling pathways that are blocked by P2 antagonists. Human, compared to rat, astrocytes had an increased calcium response and prolonged calcium wave propagation kinetics, suggesting that in our model system rat CNS cells are less responsive to simulated blast. Furthermore, in response to simulated blast, human CNS cells have increased expressions of a reactive astrocyte marker, glial fibrillary acidic protein (GFAP) and a protease, matrix metallopeptidase 9 (MMP-9). The conjoint increased expression of GFAP and MMP-9 and a purinergic ATP (P2) receptor antagonist reduction in calcium response identifies both potential mechanisms for sustained changes in brain function following primary bTBI and therapeutic strategies targeting abnormal astrocyte activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.