Endogenous Neural Stem/Progenitor Cells Stabilize the Cortical Microenvironment after Traumatic Brain Injury

Dixon, Kirsty J.; Theus, Michelle H.; Nelersa, Claudiu M.; Mier, José M.; Travieso, Lissette G.; Yu, Tzong-Shiue; Kernie, Steven G.; Liebl, Daniel J.

doi:10.1089/neu.2014.3390

Cited by 38 publications

(29 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While selectively ablating adult neurogenesis can dampen functional recovery [68,69], the effects on early childhood or adolescence are unclear. Sun and colleagues analyzed the morphological changes within the subgranular zone of the DG and the SVZ following LFPI using P28 juvenile and P90 adult rats [70].…”

Section: Age-at-injury Response To Preclinical Tbimentioning

confidence: 99%

Age-Dependent Responses Following Traumatic Brain Injury

Brickler¹,

Morton²,

Hazy³

et al. 2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

Self Cite

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is a growing health concern worldwide that affects a broad range of the population. As TBI is the leading cause of disability and mortality in children, several preclinical models have been developed using rodents at a variety of different ages; however, key brain maturation events are overlooked that leave some age groups more or less vulnerable to injury. Thus, there has been a large emphasis on producing relevant animal models to elucidate molecular pathways that could be of therapeutic potential to help limit neuronal injury and improve behavioral outcome. TBI involves a host of different biochemical events, including disruption of the cerebral vasculature and breakdown of the blood-brain barrier (BBB) that exacerbates secondary injuries. A better understanding of age-related mechanism(s) underlying brain injury will aid in establishing more effective treatment strategies aimed at improving restoration and preventing further neuronal loss. This review looks at studies that focus on modeling the adolescent population and highlights the importance of individualized aged therapeutics to TBI.

show abstract

Section: Age-at-injury Response To Preclinical Tbimentioning

confidence: 99%

Age-Dependent Responses Following Traumatic Brain Injury

Brickler¹,

Morton²,

Hazy³

et al. 2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

Self Cite

View full text Add to dashboard Cite

show abstract

“…104 Recently, promoting endogenous NSCs or NPCs proliferation and differentiation have been shown to stabilize the cortical microenvironment and enhance post-TBI functional recovery. [105][106][107][108] Exogenous NSC transplantation also promotes neuroprotection, enhances hippocampal neurogenesis, and improves functional outcomes. 109 In animal models, the number of cells for transplantation ranges from 0.15 to 25 million cells per kg body weight.…”

Section: Neurorestorationmentioning

confidence: 99%

Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

2016

Cell Transplant

View full text Add to dashboard Cite

Traumatic brain injury (TBI) presents in various forms ranging from mild alterations of consciousness to an unrelenting comatose state and death. In the most severe form of TBI, the entirety of the brain is affected by a diffuse type of injury and swelling. Treatment modalities vary extensively based on the severity of the injury and range from daily cognitive therapy sessions to radical surgery such as bilateral decompressive craniectomies. Guidelines have been set forth regarding the optimal management of TBI, but they must be taken in context of the situation and cannot be used in every individual circumstance. In this review article, we have summarized the current status of treatment for TBI in both clinical practice and basic research. We have put forth a brief overview of the various subtypes of traumatic injuries, optimal medical management, and both the noninvasive and invasive monitoring modalities, in addition to the surgical interventions necessary in particular instances. We have overviewed the main achievements in searching for therapeutic strategies of TBI in basic science. We have also discussed the future direction for developing TBI treatment from an experimental perspective. Keywords traumatic brain injury, management, intracranial hypertension, treatment strategies Epidemiology of Traumatic Brain Injury (TBI)TBI continues to plague millions of individuals around the world on an annual basis. According to the Centers for Disease Control, the total combined rates for TBI-related emergency department visits, hospitalizations, and deaths have increased in the decade 2001-2010. 1 However, taken individually, the number of deaths related to TBIs has decreased over this same period of time likely secondary in part to increased awareness, structuralizing management and guidelines, and significant technological advancements in current treatment regimens. We should also acknowledge that there is a certain percentage of TBIs that never reach medical care, hence, the overall rates for TBIs are likely underreported. 2The highest rates of TBI tend to be in a very young agegroup (0-4 y) as well as in adolescents and young adults (15-24 y). There is another peak in incidence in the elderly (>65 y). The 2 leading causes of TBI overall are falls and motor vehicle accidents.3 As a result of an overall increased number of TBIs, but lower rate of related deaths, we have a growing population of individuals living with significant disabilities directly related to their TBI. Pathophysiology of TBITBI pathogenesis is a complex process that results from primary and secondary injuries that lead to temporary or permanent neurological deficits. The primary deficit is related directly to the primary external impact of the brain. The secondary injury can happen from minutes to days from the primary impact and consists of a molecular, chemical, and inflammatory cascade responsible for further cerebral damage. This cascade involves depolarization of the neurons

show abstract

“…Migrating neuroblasts move in chains, where gap and adherens junctions between neighboring neuroblasts form connected movements (Lois et al, 1996; Ohab et al, 2006; Yamashita et al, 2006; Belvindrah et al, 2007; Kojima et al, 2010). After CNS injury and disease, neuroblasts have been shown to exit the RMS and migrate ectopically to sites of tissue damage (Arvidsson et al, 2002; Parent et al, 2002; Dixon et al, 2015); however, little is known about the cues that regulate ectopic migration. Outside the neurogenic regions neuroblasts have the capacity to differentiate into both neural and glial cell fates (Miragall et al, 1990; Bonfanti and Theodosis, 1994; Doetsch et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Outside the neurogenic regions neuroblasts have the capacity to differentiate into both neural and glial cell fates (Miragall et al, 1990; Bonfanti and Theodosis, 1994; Doetsch et al, 1997). In models of traumatic brain injury (TBI), migrating neuroblasts have been shown to provide beneficial effects to damaged tissues, such as the cortex, where they express trophic factors that support residential cell survival (Li et al, 2010; Dixon et al, 2015). In the absence of these cells, increased tissue damage and reduced functional recovery is observed (Dixon et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

“…In models of traumatic brain injury (TBI), migrating neuroblasts have been shown to provide beneficial effects to damaged tissues, such as the cortex, where they express trophic factors that support residential cell survival (Li et al, 2010; Dixon et al, 2015). In the absence of these cells, increased tissue damage and reduced functional recovery is observed (Dixon et al, 2015). Thus, expanding this population of cells and increasing their numbers in injured tissues can benefit functional recovery.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

EphrinB3 restricts endogenous neural stem cell migration after traumatic brain injury

et al. 2016

Self Cite

View full text Add to dashboard Cite

Traumatic brain injury (TBI) leads to a series of pathological events that can have profound influences on motor, sensory and cognitive functions. Conversely, TBI can also stimulate neural stem/progenitor cell proliferation leading to increased numbers of neuroblasts migrating outside their restrictive neurogenic zone to areas of damage in support of tissue integrity. Unfortunately, the factors that regulate migration are poorly understood. Here, we examine whether ephrinB3 functions to restrict neuroblasts from migrating outside the subventricular zone (SVZ) and rostral migratory stream (RMS).We have previously shown that ephrinB3 is expressed in tissues surrounding these regions, including the overlying corpus callosum (CC), and is reduced after controlled cortical impact (CCI) injury. Our current study takes advantage of ephrinB3 knockout mice to examine the influences of ephrinB3 on neuroblast migration into CC and cortex tissues after CCI injury. Both injury and/or ephrinB3 deficiency led to increased neuroblast numbers and enhanced migration outside the SVZ/RMS zones. Application of soluble ephrinB3-Fc molecules reduced neuroblast migration into the CC after injury and limited neuroblast chain migration in cultured SVZ explants. Our findings suggest that ephrinB3 expression in tissues surrounding neurogenic regions functions to restrict neuroblast migration outside the RMS by limiting chain migration.

show abstract

Endogenous Neural Stem/Progenitor Cells Stabilize the Cortical Microenvironment after Traumatic Brain Injury

Cited by 38 publications

References 56 publications

Age-Dependent Responses Following Traumatic Brain Injury

Age-Dependent Responses Following Traumatic Brain Injury

Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

EphrinB3 restricts endogenous neural stem cell migration after traumatic brain injury

Contact Info

Product

Resources

About