scholarly journals Blood–Brain Barrier Dysfunction in Mild Traumatic Brain Injury: Evidence From Preclinical Murine Models

2020 ◽  
Vol 11 ◽  
Author(s):  
Yingxi Wu ◽  
Haijian Wu ◽  
Xinying Guo ◽  
Brock Pluimer ◽  
Zhen Zhao
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blood Brain Barrier ◽  
Mild Traumatic Brain Injury ◽  
Brain Barrier ◽  
Murine Models ◽  
Barrier Dysfunction ◽  
Blood Brain

scholarly journals Mild traumatic brain injury/ concussion initiates an atypical astrocyte response caused by blood-brain barrier dysfunction

2021 ◽  
Author(s):  
Benjamin P Heithoff ◽  
Kijana K George ◽  
Oleksii Shandra ◽  
Stefanie Robel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blood Brain Barrier ◽  
Mild Traumatic Brain Injury ◽  
Coagulation Factor ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Genetic Ablation ◽  
Blood Brain ◽  
Secondary Damage

Mild traumatic brain injury/ concussion (mTBI) account for 70-90% of all reported TBI cases and cause long lasting neurological consequences in 10 to 40% of patients. Recent clinical studies revealed increased blood-brain barrier (BBB) permeability in mTBI patients, which correlated with secondary damage after mTBI. However, the cascade of cellular events initiated by exposure to blood-borne factors resulting in sustained damage are not fully resolved. We previously reported that astrocytes respond atypically to mTBI rapidly downregulating many proteins essential to their homeostatic function while classic scar formation does not occur. Here, we tested the hypothesis that mTBI -induced BBB damage causes atypical astrocytes through exposure to blood-borne factors. Using a mTBI mouse model, 2-photon imaging, an endothelial cell-specific genetic ablation approach, and serum-free primary astrocyte cultures, we demonstrated that areas with atypical astrocytes coincide with BBB damage and that exposure of astrocytes to plasma proteins is sufficient to initiate downregulation of astrocyte homeostatic proteins. While mTBI resulted in frequent impairment of both physical and metabolic BBB properties and leakage of small-sized blood-borne factors, deposition of the coagulation factor fibrinogen or vessel rupture were rare. Surprisingly, even months after mTBI BBB repair did not occur in areas with atypical astrocytes. Together, these findings implicate that even relatively small BBB disturbances are sustained long-term and render nearby astrocytes dysfunctional, likely at the cost of neuronal health and function.

scholarly journals Long-lasting blood-brain barrier dysfunction and neuroinflammation after traumatic brain injury

2020 ◽  
Vol 145 ◽  
pp. 105080
Author(s):  
Erwin A. van Vliet ◽  
Xavier Ekolle Ndode-Ekane ◽  
Lauri J. Lehto ◽  
Jan A. Gorter ◽  
Pedro Andrade ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain

Impairment of pericyte-endothelium crosstalk leads to blood-brain barrier dysfunction following traumatic brain injury

2019 ◽  
Vol 317 ◽  
pp. 260-270 ◽  
Author(s):  
Saurav Bhowmick ◽  
Veera D'Mello ◽  
Danielle Caruso ◽  
Alex Wallerstein ◽  
P.M. Abdul-Muneer
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain
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