Chemotropic Molecules: Guides for Axonal Pathfinding and Cell Migration During CNS Development

Physiology ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 130-136 ◽  
Author(s):  
Fernando de Castro
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Migration ◽  
Complex Pattern ◽  
Axonal Pathfinding ◽  
Cns Development ◽  
The Central Nervous System

Different molecules (netrins, semaphorins, slits) with chemotropic functions and their receptors (neogenin, DCC, neuropilins, plexins, robos) have been identified that guide axons during development of the nervous system to establish the complex pattern of connections among a large number of neurons. These molecules have been recently identified to play a role in cell migration of the central nervous system during development.

scholarly journals IL-9 Promotes Th17 Cell Migration into the Central Nervous System via CC Chemokine Ligand-20 Produced by Astrocytes

2011 ◽  
Vol 186 (7) ◽  
pp. 4415-4421 ◽  
Author(s):  
Yan Zhou ◽  
Yoshifumi Sonobe ◽  
Tomohiko Akahori ◽  
Shijie Jin ◽  
Jun Kawanokuchi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Migration ◽  
Th17 Cell ◽  
Cc Chemokine ◽  
Chemokine Ligand ◽  
The Central Nervous System ◽  
Cc Chemokine Ligand 20

scholarly journals Upregulation of lncRNA147410.3 in the Brain of Mice With Chronic Toxoplasma Infection Promoted Microglia Apoptosis by Regulating Hoxb3

2021 ◽  
Vol 15 ◽  
Author(s):  
Yongliang Wang ◽  
Ruxia Han ◽  
Zhejun Xu ◽  
Xiahui Sun ◽  
Chunxue Zhou ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Target Gene ◽  
Neuronal Cell ◽  
Scientific Basis ◽  
Cns Development ◽  
Toxoplasma Infection ◽  
Key Factor ◽  
The Central Nervous System ◽  
The Brain

Toxoplasma gondii is neurotropic and affects the function of nerve cells, while the mechanism is unclear. LncRNAs are abundantly enriched in the brain and participated in the delicate regulation of the central nervous system (CNS) development. However, whether these lncRNAs are involved in the regulation of microglia activation during the process of T. gondii infection is largely unknown. In this study, the upregulation of a novel lncRNA147410.3 (ENSMUST00000147410.3) was identified as a key factor to influence this process. The target gene of lncRNA147410.3 was predicted and identified as Hoxb3. The localization of lncRNA147410.3 in the brain and cells was proved in the nucleus of neuroglia through FISH assay. Furthermore, the function of lncRNA147410.3 on neuronal cell was confirmed that lncRNA147410.3 could affect proliferation, differentiation, and apoptosis of mouse microglia by positively regulating Hoxb3. Thus, our study explored the modulatory action of lncRNA147410.3 in T. gondii infected mouse brain, providing a scientific basis for using lncRNA147410.3 as a therapeutic target to treat neurological disorder induced by T. gondii.

Understanding the Molecular Basis of Cell Migration; Implications for Clinical Therapy in Multiple Sclerosis

1997 ◽  
Vol 92 (2) ◽  
pp. 113-122 ◽  
Author(s):  
Richard Milner
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Cell Migration ◽  
Molecular Mechanisms ◽  
Autoimmune Response ◽  
The Central Nervous System ◽  
Oligodendrocyte Precursor ◽  
Oligodendrocyte Precursors

1. Multiple sclerosis is characterized by areas of demyelination spread throughout the central nervous system, in which the myelin sheaths surrounding axons are destroyed. While therapies aimed at suppressing the autoimmune response, such as β-interferon, may prevent further damage, they cannot repair or replace the lost myelin. To this end, an additional therapy has been proposed, which involves transplanting cells of the oligodendrocyte lineage into the central nervous system. 2. The cell of interest for transplantation is the oligodendrocyte precursor because, unlike the differentiated cell, it is an intrinsically migratory and proliferative cell. In order to optimize the transplant strategy we have investigated the molecular mechanisms that control migration in vitro, so that these mechanisms might be upregulated to maximize cell migration in vivo. We have focused on the integrin family of cell adhesion molecules, known to play a fundamental role in the regulation of migration in other cell types. 3. These studies show that oligodendrocytes express a limited repertoire of integrins consisting of α6β1 and three different αv integrins. α6β1 is expressed throughout development but αv integrins show developmental regulation; differentiation is accompanied by loss of αvβ1 and upregulation of αvβ5. 4. Function-blocking studies show that oligodendrocyte precursor migration in vitro is mediated primarily by the developmentally regulated αvβ1 integrin, but not α6β1 or αvβ3. Taken together with previous evidence that cell migration can be regulated by altering integrin expression, this work suggests that modifying expression levels of αvβ1 on oligodendrocyte precursors may increase the migratory capacity of these cells. If so, this would support a future therapeutic strategy aimed at transplanting genetically modified oligodendrocyte precursors to repair widespread demyelinated lesions.

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