ArticleScience advances2024
Synergistic label-free fluorescence imaging and miRNA studies reveal dynamic human neuron-glial metabolic interactions following injury.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Viral reprogramming of neuronal metabolism captured by label-free imaging in a 3D human brain tissue model.Neurophotonics · 2026Article
- Multi-modal label-free imaging of cellular metabolism and oxidative stress in 3D brain tissue models.Communications biology · 2025Article
- Label-free nonlinear microscopy probes cellular metabolism and myelin dynamics in live tissue.Communications biology · 2025Article
- Extracellular vesicles as biomarkers for traumatic brain injury using a 3D in vitro human brain tissue model.Scientific reports · 2025Article
- Consensus guidelines for cellular label-free optical metabolic imaging: ensuring accuracy and reproducibility in metabolic profiling.Journal of biomedical optics · 2025Article
- Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.Frontiers in cellular neuroscience · 2025Review
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Authors and funding
16 authors.
Funding
Abstract
Neuron-glial cell interactions following traumatic brain injury (TBI) determine the propagation of damage and long-term neurodegeneration. Spatiotemporally heterogeneous cytosolic and mitochondrial metabolic pathways are involved, leading to challenges in developing effective diagnostics and treatments. An engineered three-dimensional brain tissue model comprising human neurons, astrocytes, and microglia is used in combination with label-free, two-photon imaging and microRNA studies to characterize metabolic interactions between glial and neuronal cells over 72 hours following impact injury. We interpret multiparametric, quantitative, optical metabolic assessments in the context of microRNA gene set analysis and identify distinct metabolic changes in neurons and glial cells. Glycolysis, nicotinamide adenine dinucleotide phosphate (reduced form) and glutathione synthesis, fatty acid synthesis, and oxidation are mobilized within glial cells to mitigate the impacts of initial enhancements in oxidative phosphorylation and fatty acid oxidation within neurons, which lack robust antioxidant defenses. This platform enables enhanced understanding of mechanisms that may be targeted to improve TBI diagnosis and treatment.
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