Related Experiment Video
Updated: Jul 11, 2025
Author Spotlight: Imaging Pericytes Post-Subarachnoid Hemorrhaging in Rodents
Published on: August 18, 2023
Mild traumatic brain injury induces pericyte detachment independent of stroke vulnerability
Bailey Whitehead1, Deborah Corbin1, Ali Albowaidey1
1Department of Neuroscience and Rockefeller Neuroscience Institute, West Virginia University, 108 Biomedical Rd, Morgantown, WV, 26506, USA.
Abstract:
Mild traumatic brain injury (mTBI) is an independent risk factor for ischemic stroke and can result in poorer outcomes- an effect presumed to involve the cerebral vasculature. Here we tested the hypothesis that mTBI-induced pericyte detachment from the cerebrovascular endothelium is responsible for worsened stroke outcomes. We performed a mild closed-head injury and/or treated C57/bl6 mice with imatinib mesylate, a tyrosine kinase inhibitor that induces pericyte detachment. The time course of pericyte detachment was assessed 7, 14, and 28 days post injury (DPI). To test the role of pericytes in TBI-induced exacerbation of ischemic stroke outcomes, we induced mTBI and/or treated mice with imatinib for one week prior to transient middle cerebral artery occlusion. We found that injury promoted pericyte detachment from the vasculature commensurate with the levels of detachment seen in imatinib-only treated animals, and that the detachment persisted for at least 14DPI, but recovered to sham levels by 28DPI. Further, mTBI, but not imatinib-induced pericyte detachment, increased infarct volume. Thus, we conclude that the transient detachment of pericytes caused by mTBI may not be sufficient to exacerbate subsequent ischemic stroke damage. These data have important implications for understanding cerebrovascular dysfunction following mTBI and potential mechanisms of increased risk for future ischemic strokes.
Insights
Mild traumatic brain injury (mTBI) does not worsen stroke outcomes by detaching pericytes. This study found mTBI-induced pericyte detachment was transient and did not increase stroke damage, suggesting other mechanisms are involved.
Area of Science:
- Neuroscience
- Vascular Biology
- Trauma Research
Background:
- Mild traumatic brain injury (mTBI) is a known risk factor for ischemic stroke.
- The underlying mechanisms linking mTBI to poorer stroke outcomes are not fully understood.
- Cerebrovascular dysfunction, particularly involving pericytes, is a potential contributor.
Purpose of the Study:
- To investigate if mTBI-induced pericyte detachment exacerbates ischemic stroke outcomes.
- To determine the time course of pericyte detachment following mTBI.
- To compare the effects of mTBI-induced versus drug-induced pericyte detachment on stroke injury.
Main Methods:
- Mice underwent mild closed-head injury (mTBI) or were treated with imatinib mesylate to induce pericyte detachment.
- Pericyte detachment was assessed at 7, 14, and 28 days post-injury.
- Ischemic stroke was induced via middle cerebral artery occlusion in mTBI and/or imatinib-treated mice.
Main Results:
- mTBI caused transient pericyte detachment, persisting up to 14 days post-injury and recovering by 28 days.
- Pericyte detachment levels after mTBI were comparable to those induced by imatinib.
- Only mTBI, not imatinib-induced pericyte detachment alone, significantly increased infarct volume after stroke.
Conclusions:
- Transient pericyte detachment following mTBI may not be sufficient to explain worsened stroke outcomes.
- These findings suggest that mTBI-related cerebrovascular dysfunction involves mechanisms beyond simple pericyte detachment.
- Understanding these mechanisms is crucial for addressing the increased risk of future ischemic strokes after mTBI.
