User:Ackeralexa/Neural stem cell
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Communication and migration
[edit]NSCs are stimulated to begin differentiation via exogenous cues from their microenvironment (stem cell niche), including interactions with neighboring cells (such as astrocytes and endothelial cells), growth factors (e.g., cytokines), and chemokines such as SDF-1 [1][2]. Under normal conditions, NSCs, referred to as Type B cells, reside within the niche in a quiescent state. These dormant cells act as a reservoir, and are activated in response to injury or other stimuli for neural regeneration and repair.
In response to injury or disease, changes in the NSC niche-- such as the release of inflammatory cytokines and upregulation of chemotactic factors-- can activate NSCs. Once activated, Type B cells can transform into proliferative Type C cells, which can divide into type A cells, known as neuroblasts. These neuroblasts have the potential to differentiate into mature neurons and migrate to specific regions in the brain, contributing to neurogenesis and the repair process[3]. This system ensures that NSCs remain dormant under normal conditions, but are activated only when necessary--such as during an injury or disease.
Some neural cells migrate from the SVZ along the rostral migratory stream (RMS) which contains a marrow-like structure with ependymal cells and astrocytes when stimulated. The ependymal cells and astrocytes form glial tubes that are used by migrating neuroblasts, providing structural support and insulation from electrical and chemical signals released from surrounding cells. The astrocytes are the primary precursors for rapid cell amplification. The neuroblasts form tight chains and migrate towards the specified site of cell damage to repair or replace neural cells. One example is a neuroblast migrating towards the olfactory bulb to differentiate into periglomerular or granule neurons which have a radial migration pattern rather than a tangential one.[3] Additionally, the formation of new blood vessels in a process called angiogenesis occurs following injury, and plays a crucial role in neuroblast migration by acting as physical scaffolds, guiding cells towards the site of injury. Further, the formation of new blood vessels upregulates the production of SDF-1α from ependymal cells. Neuroblasts are attracted to increased levels of SDF-1α through their receptor CXCR4, forming a chemokine gradient that guides migration towards the site of injury[1]. CXCR7 further contributes to this process by clearing excess SDF-1α to maintain an optimal concentration for directional NSC migration. Other factors such as microglia, which can release both beneficial and inhibitory factors, BDNF and IGF-1, also play a role in guided neural migration to the site of injury [4][5][6].
Lead
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[edit]References
[edit]- ^ a b Imitola, Jaime; Raddassi, Khadir; Park, Kook In; Mueller, Franz-Josef; Nieto, Marta; Teng, Yang D.; Frenkel, Dan; Li, Jianxue; Sidman, Richard L.; Walsh, Christopher A.; Snyder, Evan Y.; Khoury, Samia J. (2004-12-28). "Directed migration of neural stem cells to sites of CNS injury by the stromal cell-derived factor 1α/CXC chemokine receptor 4 pathway". Proceedings of the National Academy of Sciences. 101 (52): 18117–18122. doi:10.1073/pnas.0408258102. ISSN 0027-8424.
- ^ Cheng, Xi; Wang, Huibin; Zhang, Xiuchun; Zhao, Shanshan; Zhou, Zhike; Mu, Xiaopeng; Zhao, Chuansheng; Teng, Weiyu (2017). "The Role of SDF-1/CXCR4/CXCR7 in Neuronal Regeneration after Cerebral Ischemia". Frontiers in Neuroscience. 11: 590. doi:10.3389/fnins.2017.00590. ISSN 1662-4548. PMC 5662889. PMID 29123467.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Sakaguchi, M; Okano, H (2012). "Neural stem cells, adult neurogenesis, and galectin-1: From bench to bedside". Developmental Neurobiology. 72 (7): 1059–67. doi:10.1002/dneu.22023. PMID 22488739. S2CID 41548939.
- ^ Aarum, Johan; Sandberg, Kristian; Haeberlein, Samantha L. Budd; Persson, Mats A. A. (2003-12-23). "Migration and differentiation of neural precursor cells can be directed by microglia". Proceedings of the National Academy of Sciences of the United States of America. 100 (26): 15983–15988. doi:10.1073/pnas.2237050100. ISSN 0027-8424. PMC 307679. PMID 14668448.
- ^ Chiaramello, S.; Dalmasso, G.; Bezin, L.; Marcel, D.; Jourdan, F.; Peretto, P.; Fasolo, A.; De Marchis, S. (2007-10). "BDNF/ TrkB interaction regulates migration of SVZ precursor cells via PI3-K and MAP-K signalling pathways". The European Journal of Neuroscience. 26 (7): 1780–1790. doi:10.1111/j.1460-9568.2007.05818.x. ISSN 0953-816X. PMID 17883412.
{{cite journal}}: Check date values in:|date=(help) - ^ Nieto-Estévez, Vanesa; Defterali, Çağla; Vicario-Abejón, Carlos (2016). "IGF-I: A Key Growth Factor that Regulates Neurogenesis and Synaptogenesis from Embryonic to Adult Stages of the Brain". Frontiers in Neuroscience. 10: 52. doi:10.3389/fnins.2016.00052. ISSN 1662-4548. PMC 4763060. PMID 26941597.
{{cite journal}}: CS1 maint: unflagged free DOI (link)