scholarly journals Astrocyte and Oligodendrocyte Responses From the Subventricular Zone After Injury

2021 ◽  
Vol 15 ◽  
Author(s):  
Jennifer David-Bercholz ◽  
Chay T. Kuo ◽  
Benjamin Deneen
Keyword(s):  
Stem Cells ◽  
Brain Injury ◽  
Subventricular Zone ◽  
Neural Progenitor Cells ◽  
Regulatory Mechanisms ◽  
C Cells ◽  
Brain Repair ◽  
Injury Site ◽  
Cellular Processes ◽  
Different Types

Under normal conditions, neural stem cells (NSCs or B cells) in the adult subventricular zone (SVZ) give rise to amplifying neural progenitor cells (NPCs or C cells), which can produce neuroblasts (or A cells) that migrate to the olfactory bulb and differentiate into new neurons. However, following brain injury, these cells migrate toward the injury site where they differentiate into astrocytes and oligodendrocytes. In this review, we will focus on recent findings that chronicle how astrocytes and oligodendrocytes derived from SVZ-NSCs respond to different types of injury. We will also discuss molecular regulators of SVZ-NSC proliferation and their differentiation into astrocytes and oligodendrocytes. Overall, the goal of this review is to highlight how SVZ-NSCs respond to injury and to summarize the regulatory mechanisms that oversee their glial response. These molecular and cellular processes will provide critical insights needed to develop strategies to promote brain repair following injury using SVZ-NSCs.

scholarly journals Targeting Adult Neurogenesis for Poststroke Therapy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jianfei Lu ◽  
Anatol Manaenko ◽  
Qin Hu
Keyword(s):  
Stem Cells ◽  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Tissue Repair ◽  
Therapeutic Interventions ◽  
Subgranular Zone ◽  
Brain Repair ◽  
Function Recovery ◽  
Newborn Neurons ◽  
And Function

Adult neurogenesis mainly occurs at the subventricular zone (SVZ) on the walls of the lateral ventricle and the subgranular zone (SGZ) of the dentate gyrus (DG). However, the majority of newborn neurons undergo programmed cell death (PCD) during the period of proliferation, migration, and integration. Stroke activates neural stem cells (NSCs) in both SVZ and SGZ. This process is regulated by a wide variety of signaling pathways. However, the newborn neurons derived from adult neurogenesis are insufficient for tissue repair and function recovery. Thus, enhancing the endogenous neurogenesis driven by ischemia and promoting the survival of newborn neurons can be promising therapeutic interventions for stroke. Here, we present an overview of the process of adult neurogenesis and the potential of stroke-induced neurogenesis on brain repair.

scholarly journals Enriching neural stem cell and pro-healing glial phenotypes with electrical stimulation after traumatic brain injury in male rats

2020 ◽  
Author(s):  
Eunyoung Park ◽  
Johnathan G. Lyon ◽  
Melissa Alvarado-Velez ◽  
Martha I. Betancur ◽  
Nassir Mokarram ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Electrical Stimulation ◽  
Brain Injury ◽  
Neural Stem Cells ◽  
Acute Phase ◽  
Immune Cells ◽  
Male Rats ◽  
Cell Phenotype ◽  
Injury Site

AbstractTraumatic Brain Injury (TBI) by an external physical impact results in compromised brain function via undesired neuronal death. Following the injury, resident and peripheral immune cells, astrocytes, and neural stem cells (NSCs) cooperatively contribute to the recovery of the neuronal function after TBI. However, excessive pro-inflammatory responses of immune cells, and the disappearance of endogenous NSCs at the injury site during the acute phase of TBI, can exacerbate TBI progression leading to incomplete healing. Therefore, positive outcomes may depend on early interventions to control the injury-associated cellular milieu in the early phase of injury. Here, we explore electrical stimulation (ES) of the injury site in a rodent model (male Sprague-Dawley rats) to investigate its overall effect on the constituent brain cell phenotype and composition during the acute phase of TBI. Our data showed that a brief ES for 1h on day 2 of TBI promoted pro-healing phenotypes of microglia as assessed by CD206 expression and increased the population of NSCs and Nestin+ astrocytes at 7 days post-TBI. Also, ES effectively increased the number of viable neurons when compared to the unstimulated control group. Given the salience of microglia and neural stem cells for healing after TBI, our results strongly support the potential benefit of the therapeutic use of ES during the acute phase of TBI to regulate neuroinflammation and to enhance neuroregeneration.Significance StatementTraumatic brain injury (TBI) occurs when a head injury leads to a disruption of normal function in the brain and is a major cause of death and disability, worldwide. The authors used electrical stimulation during the acute phase of TBI, which promoted pro-healing phenotypes of microglia and increased the number of neural stem cells and Nestin+ astrocytes, thereby enhancing neuronal viability. These findings support further study of electrical stimulation to regulate neuroinflammation and to enhance neuroregeneration after TBI.Graphical AbstractFIGURE 1.

Neural Stem Cells in the Immature, but Not the Mature, Subventricular Zone Respond Robustly to Traumatic Brain Injury

2014 ◽  
Vol 37 (1) ◽  
pp. 29-42 ◽  
Author(s):  
Matthew T. Goodus ◽  
Alanna M. Guzman ◽  
Frances Calderon ◽  
Yuhui Jiang ◽  
Steven W. Levison
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Flow Cytometry ◽  
Brain Injury ◽  
Neural Stem Cells ◽  
Subventricular Zone ◽  
Proliferative Response ◽  
Fold Increase ◽  
Adult Brain ◽  
Neural Precursors

Pediatric traumatic brain injury is a significant problem that affects many children each year. Progress is being made in developing neuroprotective strategies to combat these injuries. However, investigators are a long way from therapies to fully preserve injured neurons and glia. To restore neurological function, regenerative strategies will be required. Given the importance of stem cells in repairing damaged tissues and the known persistence of neural precursors in the subventricular zone (SVZ), we evaluated regenerative responses of the SVZ to a focal brain lesion. As tissues repair more slowly with aging, injury responses of male Sprague Dawley rats at 6, 11, 17, and 60 days of age and C57Bl/6 mice at 14 days of age were compared. In the injured immature animals, cell proliferation in the dorsolateral SVZ more than doubled by 48 h. By contrast, the proliferative response was almost undetectable in the adult brain. Three approaches were used to assess the relative numbers of bona fide neural stem cells, as follows: the neurosphere assay (on rats injured at postnatal day 11, P11), flow cytometry using a novel 4-marker panel (on mice injured at P14) and staining for stem/progenitor cell markers in the niche (on rats injured at P17). Precursors from the injured immature SVZ formed almost twice as many spheres as precursors from uninjured age-matched brains. Furthermore, spheres formed from the injured brain were larger, indicating that the neural precursors that formed these spheres divided more rapidly. Flow cytometry revealed a 2-fold increase in the percentage of stem cells, a 4-fold increase in multipotential progenitor-3 cells and a 2.5-fold increase in glial-restricted progenitor-2/multipotential-3 cells. Analogously, there was a 2-fold increase in the mitotic index of nestin+/Mash1- immunoreactive cells within the immediately subependymal region. As the early postnatal SVZ is predominantly generating glial cells, an expansion of precursors might not necessarily lead to the production of many new neurons. On the contrary, many BrdU+/doublecortin+ cells were observed streaming out of the SVZ into the neocortex 2 weeks after injuries to P11 rats. However, very few new mature neurons were seen adjacent to the lesion 28 days after injury. Altogether, these data indicate that immature SVZ cells mount a more robust proliferative response to a focal brain injury than adult cells, which includes an expansion of stem cells, primitive progenitors and neuroblasts. Nonetheless, this regenerative response does not result in significant neuronal replacement, indicating that new strategies need to be implemented to retain the regenerated neurons and glia that are being produced.

scholarly journals Vascular niche contribution to age-associated neural stem cell dysfunction

2017 ◽  
Vol 313 (5) ◽  
pp. H896-H902 ◽  
Author(s):  
Deana M. Apple ◽  
Erzsebet Kokovay
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Dentate Gyrus ◽  
Cell Fate ◽  
Subventricular Zone ◽  
Tissue Homeostasis ◽  
Brain Repair ◽  
Vascular Plexus ◽  
Cell Dysfunction ◽  
Vascular Niche

Neural stem cells (NSCs) persist throughout life in the dentate gyrus and the ventricular-subventricular zone, where they continuously provide new neurons and some glia. These cells are found in specialized niches that regulate quiescence, activation, differentiation, and cell fate choice. A key aspect of the regulatory niche is the vascular plexus, which modulates NSC behavior during tissue homeostasis and regeneration. During aging, NSCs become depleted and dysfunctional, resulting in reduced neurogenesis and poor brain repair. In this review, we discuss the emerging evidence that changes in the vascular niche both structurally and functionally contribute to reduced neurogenesis during aging and how this might contribute to reduced plasticity and repair in the aged brain.

scholarly journals BMP4/LIF or RA/Forskolin Suppresses the Proliferation of Neural Stem Cells Derived from Adult Monkey Brain

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Xinxin Han ◽  
Liming Yu ◽  
Qingqing Chen ◽  
Min Wang ◽  
Jie Ren ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Brain Injury ◽  
Cell Therapy ◽  
Neural Stem Cells ◽  
Cell Morphology ◽  
Nonhuman Primates ◽  
Neural Progenitor Cells ◽  
Combined Treatment ◽  
Monkey Brain

Monkeys are much closer to human and are the most common nonhuman primates which are used in biomedical studies. Neural progenitor cells can originate from the hippocampus of adult monkeys. Despite a few reports, the detailed properties of monkey neural stem cells (NSCs) and their responses to cytokine are still unclear. Here, we derive NSCs from an adult monkey brain and demonstrate that BMP4 inhibits cell proliferation and affects cell morphology of monkey NSCs. Combined treatment of BMP4 and LIF or RA and Forskolin represses the proliferation of monkey NSCs. We also show that BMP4 may promote monkey NSC quiescence. Our study therefore provides implications for NSC-based cell therapy of brain injury in the future.

scholarly journals Enhanced Homing of Mesenchymal Stem Cells Overexpressing Fibroblast Growth Factor 21 to Injury Site in a Mouse Model of Traumatic Brain Injury

2019 ◽  
Vol 20 (11) ◽  
pp. 2624 ◽  
Author(s):  
Rami Ahmad Shahror ◽  
Ahmed Atef Ahmed Ali ◽  
Chung-Che Wu ◽  
Yung-Hsiao Chiang ◽  
Kai-Yun Chen
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Brain Injury ◽  
Growth Factor ◽  
Real Time ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Injury Site ◽  
Non Invasive

Mesenchymal stem cells (MSCs) are emerging as a potential therapeutic intervention for brain injury due to their neuroprotective effects and safe profile. However, the homing ability of MSCs to injury sites still needs to be improved. Fibroblast Growth Factor 21 (FGF21) was recently reported to enhance cells migration in different cells type. In this study, we investigated whether MSCs that overexpressing FGF21 (MSC-FGF21) could exhibit enhanced homing efficacy in brain injury. We used novel Molday IONEverGreen™ (MIEG) as cell labeling probe that enables a non-invasive, high-sensitive and real-time MRI tracking. Using a mouse model of traumatic brain injury (TBI), MIEG labeled MSCs were transplanted into the contralateral lateral ventricle followed by real-time MRI tracking. FGF21 retained MSC abilities of proliferation and morphology. MSC-FGF21 showed significantly greater migration in transwell assay compared to control MSC. MIEG labeling showed no effects on MSCs’ viability, proliferation and differentiation. Magnetic resonance imaging (MRI) revealed that FGF21 significantly enhances the homing of MSC toward injury site. Histological analysis further confirmed the MRI findings. Taken together, these results show that FGF21 overexpression and MIEG labeling of MSC enhances their homing abilities and enables non-invasive real time tracking of the transplanted cells, provides a promising approach for MSC based therapy and tracking in TBI.

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