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LPS Treatment Alters Oligodendrocyte Precursor Cell Migration

The etiology of multiple sclerosis (MS), is characterized by the immune system attacking specialized cells within the central nervous system known as oligodendrocytes. Cytosolic projections of oligodendrocytes wrap their processes around axons to insulate them so that fast salutatory conduction of action potentials can occur. However, in MS, myelin is damaged, compromising axonal integrity and salutatory conduction. This destruction is thought to be a combination of many factors such as activation of inflammatory pathways and epigenetic mechanisms. One of the inflammatory pathways that is thought to be involved in the disease pathology of MS is the Toll‐like receptor (TLR) pathway that leads to the release of pro‐inflammatory cytokines such as TNF‐alpha, NFkB, and series of ILs. Together, these pro‐inflammatory cytokines have been shown to cause cells to undergo apoptosis and cell death. Moreover, it has been found in previous studies that there is increased TLR expression in the lesions of MS patients as well as Experimental Autoimmune Encephalomyelitis, which is an animal model used to study MS and other demyelinating diseases. Along with increased TLR expression in MS lesions, DNA methylation changes, such as increased hypermethylation and demethylation have also been found. Although there have been studies looking into TLRs and DNA methylation in MS lesions, understanding the mechanisms of TLRs in the development of new myelin during remyelination needs to be studied. Previously, we found that using lipopolysaccharide (LPS) to activate TLR2 and TLR4 in induced pluripotent stem cells (iPS) derived oligodendrocyte precursor cells (OPCs) resulted in the demethylation of several genes associated with neural and stem cell migration. In this study, we analyzed if TLR2 and TLR4 activation alters OPC migration. To do this, we performed a chemotactic assay in LPS and 5‐Azacytidine treated OPCs and found that TLR2 and TLR4 activation, along with inhibited methylation, results in increased OPC migration.