Oligodendrocyte progenitor cells (OPCs) are a subtype of glia giving rise to the myelin-producing cells in the central nervous system. Highly dividing cells during the embryogenesis, OPCs become relatively quiescent in adulthood, where they represent an important source of potential remyelinating oligodendrocytes upon injury. During their differentiation, OPCs make contacts with other glial cells and neurons with which they can form synapses and gap junctions, and they continuously refine their intrinsic program based on the extracellular cues. Neurotransmitters, axonal signals, morphogens, cytokines, and extracellular matrix proteins can change the fate of OPCs, modulate their maturation timing, promote their local migration, or keep them undifferentiated to maintain a pool of proliferating cells. The cellular and molecular context makes OPCs highly heterogeneous and plastic both in time and space with mechanisms largely unknown.
What kind of information do OPCs receive from the environment? To what extent is their physiological differentiation determined by the nearby cells? Do OPCs simply generate mature oligodendrocytes and eventually new myelin or they can also intervene in other processes? What are the triggers that interrupt adult OPC quiescence? In this Research Topic, we will address some of these issues focusing on the different behavior of OPCs in response to the multitude of signals both in physiological and pathological conditions.
The Research Topic welcomes Original Research articles and Reviews focusing, but not limited to:
- Novel phenomena of cell-to-cell communication;
- Novel signals driving maturation, myelination, or remyelination during disease;
- Synthetic or natural compounds acting on OPCs;
- Effects of extracellular vesicles and their components (protein, lipids, microRNAs) on OPC physiology and pathology;
- Molecular consequence of the physical interaction with neurons, glial cells, extracellular matrix, cerebral vessels, components of the blood-brain barrier;
- Extracellular environment and mechanosensitivity;
- Chemoattraction and chemorepulsion;
- Response to acute or chronic inflammatory signals;
- Signals that shift the fate of OPCs to non-oligodendroglial cells;
- Factors influencing OPC metabolism;
- Progressive loss of responsiveness during aging;
- Circadian rhythms and OPC behavior;
- Factors contributing to regional heterogeneity.
Oligodendrocyte progenitor cells (OPCs) are a subtype of glia giving rise to the myelin-producing cells in the central nervous system. Highly dividing cells during the embryogenesis, OPCs become relatively quiescent in adulthood, where they represent an important source of potential remyelinating oligodendrocytes upon injury. During their differentiation, OPCs make contacts with other glial cells and neurons with which they can form synapses and gap junctions, and they continuously refine their intrinsic program based on the extracellular cues. Neurotransmitters, axonal signals, morphogens, cytokines, and extracellular matrix proteins can change the fate of OPCs, modulate their maturation timing, promote their local migration, or keep them undifferentiated to maintain a pool of proliferating cells. The cellular and molecular context makes OPCs highly heterogeneous and plastic both in time and space with mechanisms largely unknown.
What kind of information do OPCs receive from the environment? To what extent is their physiological differentiation determined by the nearby cells? Do OPCs simply generate mature oligodendrocytes and eventually new myelin or they can also intervene in other processes? What are the triggers that interrupt adult OPC quiescence? In this Research Topic, we will address some of these issues focusing on the different behavior of OPCs in response to the multitude of signals both in physiological and pathological conditions.
The Research Topic welcomes Original Research articles and Reviews focusing, but not limited to:
- Novel phenomena of cell-to-cell communication;
- Novel signals driving maturation, myelination, or remyelination during disease;
- Synthetic or natural compounds acting on OPCs;
- Effects of extracellular vesicles and their components (protein, lipids, microRNAs) on OPC physiology and pathology;
- Molecular consequence of the physical interaction with neurons, glial cells, extracellular matrix, cerebral vessels, components of the blood-brain barrier;
- Extracellular environment and mechanosensitivity;
- Chemoattraction and chemorepulsion;
- Response to acute or chronic inflammatory signals;
- Signals that shift the fate of OPCs to non-oligodendroglial cells;
- Factors influencing OPC metabolism;
- Progressive loss of responsiveness during aging;
- Circadian rhythms and OPC behavior;
- Factors contributing to regional heterogeneity.
