Severe traumatic brain injury temporally affects cerebral blood flow, endothelial cell phenotype, and cilia
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View abstract on PubMed
Summary
This summary is machine-generated.Severe traumatic brain injury (sTBI) disrupts cerebral blood flow (CBF), leading to hypoxia and loss of the ciliary protein ARL13B in brain endothelial cells (ECs). This study reveals molecular changes in ECs and their cilia following sTBI.
Area Of Science
- Neuroscience
- Cell Biology
- Biomedical Engineering
Background
- Altered cerebral blood flow (CBF) in severe traumatic brain injury (sTBI) is linked to poor executive function.
- The molecular impact of altered CBF on endothelial cells (ECs) and their cilia in sTBI remains unknown.
Purpose Of The Study
- Investigate the molecular consequences of altered CBF on brain ECs and their cilia after sTBI.
- Determine the role of hypoxia in regulating ciliary protein expression in ECs post-injury.
Main Methods
- Utilized laser speckle contrast imaging and single-cell RNA sequencing (scRNAseq) in a mouse model of sTBI.
- Performed flow cytometry for protein validation and in vitro experiments to model hypoxic conditions.
- Analyzed gene and protein expression changes in ECs, focusing on the ciliary protein ARL13B.
Main Results
- sTBI caused immediate and sustained reductions in CBF in both impacted and non-impacted brain regions.
- scRNAseq revealed altered proportions of EC sub-clusters and differential gene expression related to fluid shear stress and hypoxia.
- Loss of ciliary gene Arl13b expression and ARL13B protein was observed in brain ECs as early as day 1 post-injury, with ARL13B detected in peripheral blood.
Conclusions
- Disrupted CBF in sTBI creates a hypoxic environment affecting brain ECs.
- Hypoxia influences ciliary gene and protein expression in ECs, specifically impacting ARL13B levels post-injury.
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