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Updated: Jun 25, 2026

Stretch in Brain Microvascular Endothelial Cells cEND as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier
Published on: October 26, 2013
Metabolomic alterations in human brain microvascular endothelial cells induced by traumatic injury
Enis Cela1,2, David Tweddell3, Eric K Patterson1
1London Health Sciences Centre Research Institute, London, ON, Canada.
Introduction:
Altered metabolic pathways are critical in the progression of traumatic brain injury (TBI). Identifying differentially abundant metabolites (DAMs) from specific cell types can offer valuable diagnostic and prognostic insights.
Objective:
This study aimed to characterize the metabolomic profile of injured human brain microvascular endothelial cells (hBMEC) at 2-, 12-, 24-, and 48 h post-injury.
Methods:
Using an in vitro TBI model, we analyzed metabolites in cell culture media through a combination of direct injection mass spectrometry and a custom reverse-phase LC-MS/MS assay. We evaluated 644 metabolites at each time point.
Results:
Phosphatidylcholines were significantly upregulated across all time intervals. At 2- and 12 h post-injury, the most significantly upregulated metabolites included sphingomyelin (OH) C22:1, ethylmalonic acid, and methylhistidine, while guanosine and the combination of butyric acid + isobutyric acid were the most downregulated. At 24 and 48 h, deoxyadenosine and inosine, respectively, emerged as the most upregulated metabolites, with butyric acid + isobutyric acid and quinoline-4-carboxylic acid showing the greatest downregulation.
Conclusion:
Metabolomic profiling identified various DAMs after traumatic injury that are linked to human endothelial dysfunction. Future experiments should expand the number of metabolites measured to determine the underlying signaling pathways.
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