Control of axonophilic migration of oligodendrocyte precursor cells by Eph–ephrin interaction

2004 ◽  
Vol 1 (1) ◽  
pp. 73-83 ◽  
Author(s):  
LAETITIA PRESTOZ ◽  
ELLI CHATZOPOULOU ◽  
GREGORY LEMKINE ◽  
NATHALIE SPASSKY ◽  
BARBARA LEBRAS ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cells ◽  
Precursor Cells ◽  
Eph Receptors ◽  
Retinal Ganglion ◽  
Oligodendrocyte Precursor Cells ◽  
Matrix Cell ◽  
Ephb Receptors ◽  
Ephrin Ligands ◽  
Oligodendrocyte Precursor

The migration of oligodendrocyte precursor cells (OPCs) is modulated by secreted molecules in their environment and by cell–cell and matrix–cell interactions. Here, we ask whether membrane-anchored guidance cues, such as the ephrin ligands and their Eph receptors, participate in the control of OPC migration in the optic nerve. We postulate that EphA and EphB receptors, which are expressed on axons of retinal ganglion cells, interact with ephrins on the surface of OPCs. We show the expression of ephrinA5, ephrinB 2 and ephrinB3 in the migrating OPCs of the optic nerve as well as in the diencephalic sites from where they originate. In addition, we demonstrate that coated EphB2-Fc receptors, which are specific for ephrinB2/B3 ligands, induce dramatic changes in the contact and migratory properties of OPCs, indicating that axonal EphB receptors activate ephrinB signaling in OPCs. Based on these findings, we propose that OPCs are characterized by an ephrin code, and that Eph–ephrin interactions between axons and OPCs control the distribution of OPCs in the optic axonal tracts, and the progress and arrest of their migration.

scholarly journals Oligodendrocyte precursor cells in the mouse optic nerve originate in the preoptic area

2017 ◽  
Vol 222 (5) ◽  
pp. 2441-2448 ◽  
Author(s):  
Katsuhiko Ono ◽  
Kengo Yoshii ◽  
Hiroyuki Tominaga ◽  
Hitoshi Gotoh ◽  
Tadashi Nomura ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Preoptic Area ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor

scholarly journals Oligodendrocyte Precursor Cells Sculpt the Visual System by Regulating Axonal Remodeling

2021 ◽  
Author(s):  
Yan Xiao ◽  
Laura J Hoodless ◽  
Luigi Petrucco ◽  
Ruben Portugues ◽  
Tim Czopka
Keyword(s):  
Neural Circuit ◽  
Precursor Cells ◽  
Retinal Ganglion ◽  
Oligodendrocyte Precursor Cells ◽  
Precise Control ◽  
Oligodendrocyte Precursor ◽  
Zebrafish Optic Tectum ◽  
And Function ◽  
Fine Tune ◽  
Ganglion Cell Axon

Many oligodendrocyte precursor cells (OPCs) do not differentiate to form myelin, suggesting additional roles of this cell population. The zebrafish optic tectum contains OPCs in regions devoid of myelin. Elimination of these OPCs impaired precise control of retinal ganglion cell axon arbor size during formation and maturation of retinotectal connectivity, and in consequence impaired visual acuity. Therefore, OPCs fine-tune neural circuit structure and function independently of their canonical role to make myelin.

scholarly journals Long-Term Culture of Purified Postnatal Oligodendrocyte Precursor Cells

2000 ◽  
Vol 148 (5) ◽  
pp. 971-984 ◽  
Author(s):  
Dean G. Tang ◽  
Yasuhito M. Tokumoto ◽  
Martin C. Raff
Keyword(s):  
Optic Nerve ◽  
Growth Factor ◽  
Precursor Cells ◽  
Platelet Derived Growth Factor ◽  
Oligodendrocyte Precursor Cells ◽  
Serum Free Medium ◽  
Free Medium ◽  
Oligodendrocyte Precursor ◽  
Vertebrate Central Nervous System

Oligodendrocytes myelinate axons in the vertebrate central nervous system (CNS). They develop from precursor cells (OPCs), some of which persist in the adult CNS. Adult OPCs differ in many of their properties from OPCs in the developing CNS. In this study we have purified OPCs from postnatal rat optic nerve and cultured them in serum-free medium containing platelet-derived growth factor (PDGF), the main mitogen for OPCs, but in the absence of thyroid hormone in order to inhibit their differentiation into oligodendrocytes. We find that many of the cells continue to proliferate for more than a year and progressively acquire a number of the characteristics of OPCs isolated from adult optic nerve. These findings suggest that OPCs have an intrinsic maturation program that progressively changes the cell's phenotype over many months. When we culture the postnatal OPCs in the same conditions but with the addition of basic fibroblast growth factor (bFGF), the cells acquire these mature characteristics much more slowly, suggesting that the combination of bFGF and PDGF, previously shown to inhibit OPC differentiation, also inhibits OPC maturation. The challenge now is to determine the molecular basis of such a protracted maturation program and how the program is restrained by bFGF.

Melatonin As a Modulator of Degenerative and Regenerative Signaling Pathways in Injured Retinal Ganglion Cells

2019 ◽  
Vol 25 (28) ◽  
pp. 3057-3073 ◽  
Author(s):  
Kobra B. Juybari ◽  
Azam Hosseinzadeh ◽  
Habib Ghaznavi ◽  
Mahboobeh Kamali ◽  
Ahad Sedaghat ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathways ◽  
Retinal Ganglion Cells ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Ganglion Cells ◽  
Axon Growth ◽  
Nerve Fibers ◽  
Retinal Ganglion

Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance, etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including optic neuropathies. Based on the information provided in this review, melatonin may act as a promising agent to reduce RGC death in various retinal pathologic conditions.

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