Regulation of Subventricular Zone-Derived Cells Migration in the Adult Brain

Capilla-González, Vivian; Lavell, Emily; Quiñones‐Hinojosa, Alfredo; Guerrero-Cázares, Hugo

doi:10.1007/978-3-319-16537-0_1

Cited by 33 publications

(22 citation statements)

References 143 publications

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“…The VMC forms an array that is structurally similar to the rostral migratory stream of the lateral ventricles; indeed, several disperse, pinwheel-like structures were detected (Fig. 3D and F), similar structures are associated with adult active neurogenic niches in the lateral ventricles153435; however, as previously shown, no evidence of active cell proliferation was detected. Further studies will be necessary to determine the role of these organizational features in this area of the cerebellum.…”

Section: Discussionsupporting

confidence: 72%

Identification of novel cellular clusters define a specialized area in the cerebellar periventricular zone

González-González

Gómez-González

Becerra-González

et al. 2017

Sci Rep

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The periventricular zone of cerebellum is a germinative niche during the embryonic development, nevertheless its structural organization and functional implications in adult have not been widely studied. Here we disclose the presence of two novel clusters of cells in that area. The first one was named the subventricular cellular cluster (SVCC) and is composed of cells that express glial and neuronal markers. The second was named the ventromedial cord (VMC) and appears as a streak of biciliated cells with microvillosities facing the ventricle, that includes GFAP+ and nestin+ cells organized along the periventricular vasculature. The dorsal limit of the SVCC is associated with myelinated axons of neurons of unknown origin. This paper describes the characteristics and organization of these groups of cells. They can be observed from late embryonic development in the transgenic mouse line GFAP-GFP. The SVCC and VMC expand during early postnatal development but are restricted to the central area of the ventricle in adulthood. We did not find evidence of cell proliferation, cell migration or the presence of fenestrated blood vessels. These findings provide new insights into the knowledge of the cellular composition and structural organization of the periventricular zone of cerebellum.

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Section: Discussionsupporting

confidence: 72%

Identification of novel cellular clusters define a specialized area in the cerebellar periventricular zone

González-González

Gómez-González

Becerra-González

et al. 2017

Sci Rep

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“…60,94 Newly generated neuroblasts in the subventricular zone can migrate to the injured area and become mature neurons after TBI. 11,17,26 AcSDKP not only significantly reduced neuronal cell loss in the hippocampus, but also increased the number of newly born neurons and dendritic spines, which may contribute to the memory recovery after TBI. Additionally, cortical lesion volume of brain was significantly reduced with AcSDKP treatment initiated 1 hour after TBI, which is consistent with our previous study showing that Tβ4 administered 6 hours after TBI significantly reduced lesion volume.…”

Section: Discussionmentioning

confidence: 91%

Treatment of traumatic brain injury in rats with N-acetyl-seryl-aspartyl-lysyl-proline

Zhang¹,

Zhang

Chopp

et al. 2017

JNS

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OBJECT Our previous studies have suggested that thymosin beta 4 (Tβ4), a major actin-sequestering protein, improves functional recovery after neural injury. N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is an active peptide fragment of Tβ4 and its effect as a treatment of traumatic brain injury (TBI) has not been investigated. Thus, this study was designed to determine whether AcSDKP treatment improves functional recovery in rats after TBI. METHODS Young adult male Wistar rats with TBI were randomly divided into the following groups: (1) Sham group (no injury); (2) Vehicle group (0.01N acetic acid); (3) AcSDKP (0.8 mg/kg/day). TBI was induced by controlled cortical impact over the left parietal cortex. AcSDKP or vehicle was administered subcutaneously starting at 1 hour post injury and continuously for 3 days using an osmotic minipump. Sensorimotor function and spatial learning were assessed using a modified neurological severity score and Morris water maze tests, respectively. Some of the animals were sacrificed 1 day after injury and their brains were processed for measurement of fibrin accumulation and neuroinflammation signaling pathways. The remaining animals were sacrificed 35 days after injury and brain sections were processed for measurement of lesion volume, hippocampal cell loss, angiogenesis, neurogenesis and dendritic spine remodeling. RESULTS Compared to the vehicle treatment, AcSDKP treatment initiated 1 hour post injury significantly improved sensorimotor functional recovery (Days 7–35, p<0.05) and spatial learning (Days 33–35, p<0.05), reduced cortical lesion volume, and hippocampal neuronal cell loss, reduced fibrin accumulation and activation of microglia/macrophages, enhanced angiogenesis and neurogenesis, and increased the number of dendritic spines in the injured brain (p<0.05). AcSDKP treatment also significantly inhibited the transforming growth factor β1/nuclear factor-kappa B signaling pathway. CONCLUSIONS AcSDKP treatment initiated 1 hour post injury provides neuroprotection and neurorestoration after TBI, indicating that this small tetrapeptide has promising therapeutic potential for treatment of TBI. Further investigation of the optimal dose and therapeutic window of AcSDKP treatment for TBI and the associated underlying mechanisms, are therefore warranted.

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“…In vivo, endogenous NPC migration is regulated by a complex interaction of internal and external factors. 16 While chemokines such as CXCL12 and SLIT2 are known to guide directional migration of NPCs, chemotaxis in the complex tissue environment is difficult to understand and investigate. [6][7][8][9] There are several factors that complicate the understanding of chemotaxis in vivo.…”

Section: Chemokine Gradients In Brain-on-a-chip Platform Induce Specimentioning

confidence: 99%

Brain-on-a-chip model enables analysis of human neuronal differentiation and chemotaxis

et al. 2016

Self Cite

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Migration of neural progenitors in the complex tissue environment of the central nervous system is not well understood. Progress in this area has the potential to drive breakthroughs in neuroregenerative therapies, brain cancer treatments, and neurodevelopmental studies. To a large extent, advances have been limited due to a lack of controlled environments recapitulating characteristics of the central nervous system milieu.Reductionist cell culture models are frequently too simplistic, and physiologically more relevant approaches such as ex vivo brain slices or in situ experiments provide little control and make information extraction difficult. Here, we present a brain-on-chip model that bridges the gap between cell culture and ex vivo/ in vivo conditions through recapitulation of self-organized neural differentiation. We use a new multi-layer silicone elastomer device, over the course of four weeks to differentiate pluripotent human (NTERA2) cells into neuronal clusters interconnected with thick axonal bundles and interspersed with astrocytes, resembling the brain parenchyma. Neurons within the device express the neurofilament heavy (NF200) mature axonal marker and the microtubule-associated protein (MAP2ab) mature dendritic marker, demonstrating that the devices are sufficiently biocompatible to allow neuronal maturation. This neuronal-glial environment is interfaced with a layer of human brain microvascular endothelial cells showing characteristics of the blood-brain barrier including the expression of zonula occludens (ZO1) tight junctions and increased trans-endothelial electrical resistance. We used this device to model migration of human neural progenitors in response to chemotactic cues within a brain-tissue setting. We show that in the presence of an environment mimicking brain conditions, neural progenitor cells show a significantly enhanced chemotactic response towards shallow gradients of CXCL12, a key chemokine expressed during embryonic brain development and in pathological tissue regions of the central nervous system. Our brain-on-chip model thus provides a convenient and scalable model of neural differentiation and maturation extensible to analysis of complex cell and tissue behaviors.

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Regulation of Subventricular Zone-Derived Cells Migration in the Adult Brain

Cited by 33 publications

References 143 publications

Identification of novel cellular clusters define a specialized area in the cerebellar periventricular zone

Identification of novel cellular clusters define a specialized area in the cerebellar periventricular zone

Treatment of traumatic brain injury in rats with N-acetyl-seryl-aspartyl-lysyl-proline

Brain-on-a-chip model enables analysis of human neuronal differentiation and chemotaxis

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