Mechanisms of cell–cell interaction in oligodendrogenesis and remyelination after stroke

Abstract

White matter damage is a clinically important aspect of several central nervous system diseases, including stroke. Cerebral white matter primarily consists of axonal bundles ensheathed with myelin secreted by mature oligodendrocytes, which play an important role in neurotransmission between different areas of gray matter. During the acute phase of stroke, damage to oligodendrocytes leads to white matter dysfunction through the loss of myelin. On the contrary, during the chronic phase, white matter components promote an environment, which is favorable for neural repair, vascular remodeling, and remyelination. For effective remyelination to take place, oligodendrocyte precursor cells (OPCs) play critical roles by proliferating and differentiating into mature oligodendrocytes, which help to decrease the burden of axonal injury. Notably, other types of cells contribute to these OPC responses under the ischemic conditions. This mini-review summarizes the non-cell autonomous mechanisms in oligodendrogenesis and remyelination after white matter damage, focusing on how OPCs receive support from their neighboring cells.

Interplay between exercise and dietary fat modulates myelinogenesis in the central nervous system

“…Myelin loss is a key pathophysiological component of neurological injury and disease, including multiple sclerosis, traumatic brain and spinal cord injury, stroke and certain neuropsychiatric disorders (Almad et al 2011; Armstrong et al 2015; Franklin and Goldman 2015; Itoh et al 2015). The loss of myelin is also a recognized part of normal ageing and a risk factor in obesity contributing to cognitive and sensorimotor decline (Kullmann et al 2015).…”

The Neural Cell Adhesion Molecule-Derived (NCAM)-Peptide FG Loop (FGL) Mobilizes Endogenous Neural Stem Cells and Promotes Endogenous Regenerative Capacity after Stroke

“…Remyelination is the main therapeutic approach for the treatment of inflammatory CNS disease such as multiple sclerosis (Chamberlain et al 2015) as well as spinal cord injury and traumatic brain injury (Bhatt et al 2014;Armstrong et al 2016). More specifically, oligodendrocyte precursors occur after stroke, mature to myelinating oligodendrocytes, and help restoring damaged white matter (Itoh et al 2015). Thus, we suggest a substantial therapeutic potential of FGL by promoting remyelination of focal brain lesions.…”

Protecting Oligodendrocytes by Targeting Non-Glutamate Receptors as a New Therapeutic Strategy for Ischemic Stroke

“…Substances such as growth factors, cytokines, and chemokines activate OPCs and induce remyelination after stroke [6,40]. These substances may also have the potential to be developed into drugs for ischemic stroke.…”

“…Cerebral WM is comprised primarily of axonal bundles that are ensheathed with myelin, an electrically insulating phospholipid layer produced by oligodendrocytes (OLGs). In recent years, increasing studies have contributed to a greater understanding of the importance of OLGs in ischemic stroke [5,6]. Thus, it is essential to support the entire neurovascular unit; the protection of OLGs, as well as neurons, should be a primary consideration for drug development in ischemic stroke.…”