Adult neurogenesis and brain remodelling after brain injury: From bench to bedside?

Quintard, Hervé; Heurteaux, Catherine; Ichaï, Carole

doi:10.1016/j.accpm.2015.02.008

Cited by 6 publications

(2 citation statements)

References 103 publications

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“…This may be one of the reasons for the enlargement of the lateral ventricles observed in Hpx-deleted mice. Moreover, it is widely accepted that neuroblasts generated in the SVZ not only migrate to the OB, but also migrate into areas that are not normally neurogenic, for example, the striatum and cerebral cortex 36 – 38 . Increased apoptosis of SVZ stem cells may also lead to a reduction in the total number of cells in these areas, which then result in a thinner cerebral cortex and the enlargement of the lateral ventricles.…”

Section: Discussionmentioning

confidence: 99%

Hemopexin is required for adult neurogenesis in the subventricular zone/olfactory bulb pathway

et al. 2018

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The neural stem cells (NSCs) of the subventricular zone (SVZ) reside within a specialized niche critical for neurogenesis. Hemopexin, a plasma glycoprotein, has been extensively studied as a heme scavenger at the systemic level. However, little is known about its function in the central nervous system, especially in neurogenesis. In the present study, we demonstrate that deletion of hemopexin leads to neurogenic abnormalities in the SVZ/olfactory bulb (OB) pathway. The lateral ventricle is enlarged in hemopexin-deficient mice, and more apoptosis was observed in Dcx+ cells. Lineage differentiation of NSCs was also inhibited in the SVZ of hemopexin-deficient mice, with more stem cells stayed in an undifferentiated, GFAP+ radial glia-like cell stage. Moreover, hemopexin deletion resulted in impaired neuroblast migration in the rostral migratory stream. Furthermore, exogenous hemopexin protein inhibited apoptosis and promoted the migration and differentiation of cultured NSCs. Finally, immunohistochemical analysis demonstrated that deletion of hemopexin reduced the number of interneurons in the OB. Together, these results suggest a new molecular mechanism for the NSC niche that regulates adult neurogenesis in the SVZ/OB pathway. Our findings may benefit the understanding for olfactory system development.

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Section: Discussionmentioning

confidence: 99%

Hemopexin is required for adult neurogenesis in the subventricular zone/olfactory bulb pathway

et al. 2018

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“…The main mechanisms of vascular repair after TBI are angiogenesis and vasculogenesis, which contribute to the development of a primitive vasculature during the embryonic phase and promote vascular repair in adulthood following TBI. These intricate yet distinct processes play a crucial role in repairing the damaged vasculature following TBI [ 74 , 75 ]. Angiogenesis is characterized by EC proliferation, migration, tube formation, branching and anastomosis [ 76 ].…”

Section: Reviewmentioning

confidence: 99%

Cellular and molecular mechanisms in vascular repair after traumatic brain injury: a narrative review

Zhao,

Yan,

Wen

et al. 2023

Burns &Amp; Trauma

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Traumatic brain injury (TBI) disrupts normal brain function and is associated with high morbidity and fatality rates. TBI is characterized as mild, moderate or severe depending on its severity. The damage may be transient and limited to the dura matter, with only subtle changes in cerebral parenchyma, or life-threatening with obvious focal contusions, hematomas and edema. Blood vessels are often injured in TBI. Even in mild TBI, dysfunctional cerebral vascular repair may result in prolonged symptoms and poor outcomes. Various distinct types of cells participate in vascular repair after TBI. A better understanding of the cellular response and function in vascular repair can facilitate the development of new therapeutic strategies. In this review, we analyzed the mechanism of cerebrovascular impairment and the repercussions following various forms of TBI. We then discussed the role of distinct cell types in the repair of meningeal and parenchyma vasculature following TBI, including endothelial cells, endothelial progenitor cells, pericytes, glial cells (astrocytes and microglia), neurons, myeloid cells (macrophages and monocytes) and meningeal lymphatic endothelial cells. Finally, possible treatment techniques targeting these unique cell types for vascular repair after TBI are discussed.

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Cellular Therapy for Spinal Muscular Atrophy

Faravelli

Corti

2017

Molecular and Cellular Therapies for Motor Neuron Diseases

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Adult neurogenesis and brain remodelling after brain injury: From bench to bedside?

Cited by 6 publications

References 103 publications

Hemopexin is required for adult neurogenesis in the subventricular zone/olfactory bulb pathway

Hemopexin is required for adult neurogenesis in the subventricular zone/olfactory bulb pathway

Cellular and molecular mechanisms in vascular repair after traumatic brain injury: a narrative review

Cellular Therapy for Spinal Muscular Atrophy

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