Response of the cerebral vasculature following traumatic brain injury

Abstract

The critical role of the vasculature and its repair in neurological disease states is beginning to emerge particularly for stroke, dementia, epilepsy, Parkinson's disease, tumors and others. However, little attention has been focused on how the cerebral vasculature responds following traumatic brain injury (TBI). TBI often results in significant injury to the vasculature in the brain with subsequent cerebral hypoperfusion, ischemia, hypoxia, hemorrhage, blood-brain barrier disruption and edema. The sequalae that follow TBI result in neurological dysfunction across a host of physiological and psychological domains. Given the importance of restoring vascular function after injury, emerging research has focused on understanding the vascular response after TBI and the key cellular and molecular components of vascular repair. A more complete understanding of vascular repair mechanisms are needed and could lead to development of new vasculogenic therapies, not only for TBI but potentially vascular-related brain injuries. In this review, we delineate the vascular effects of TBI, its temporal response to injury and putative biomarkers for arterial and venous repair in TBI. We highlight several molecular pathways that may play a significant role in vascular repair after brain injury.

Cortical Transplantation of Brain‐Mimetic Glycosaminoglycan Scaffolds and Neural Progenitor Cells Promotes Vascular Regeneration and Functional Recovery after Ischemic Stroke in Mice

“…The secreted mitogen bFGF in particular plays an important role in brain repair after injury by promoting proliferation, migration, and survival of endothelial cells . Furthermore, bFGF also stimulates production of vascular endothelial growth factor (VEGF) which acts in conjunction with bFGF to promote angiogenesis . Arteriogenesis and pial collateral vascular remodeling are also carried out by bFGF signaling after cerebral ischemia …”

“…[30] Furthermore, bFGF also stimulates production of vascular endothelial growth factor (VEGF) which acts in conjunction with bFGF to promote angiogenesis. [27,31] Arteriogenesis and pial collateral vascular remodeling are also carried out by bFGF signaling after cerebral ischemia. [30,32,33] Previous studies have demonstrated that CS-A can support neural stem cells in vitro and transplanted cells in vivo following traumatic brain injury.…”

A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?

“…Increased microvascular permeability is thought to occur via downregulation and/or degradation/ubiquination of tight junction proteins [211-213], and angiogenesis via recruitment of endothelial progenitor cells [214]. VEGF-A is activated by MMP-9, and similarly is also involved in neurogenesis and repair [215], thus making the timing of modulation important to any potential benefit on edema/outcome [80].…”

Inhibition of Lats1/p‐YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of traumatic brain injury

“…During TBI, neuronal cell death is not only a paramount contributor to neurological deficits but also a critical factor which seriously affecting the TBI patients’ quality of life. And the neuronal apoptosis after TBI often caused by some secondary events such as hemorrhage, brain edema, and local inflammation . Although there are a significant amount of studies about TBI, there are few effective clinical treatments for TBI patients .…”

“…And the neuronal apoptosis after TBI often caused by some secondary events such as hemorrhage, brain edema, and local inflammation. [2][3][4] Although there are a significant amount of studies about TBI, there are few effective clinical treatments for TBI patients. 5 Inadequate understanding of the pathogenesis of neuronal cell death in the damaged area and its surroundings is a major obstacle to the effective treatment of TBI.…”