MicroRNA Partially Restores Myelination, Limb Function in Multiple Sclerosis
Study finds miR-219 restarts myelin production in nerves of mice with multiple sclerosis.
Treatment with a microRNA restarted myelin production in mice with multiple sclerosis (MS) and restored limb mobility, according to a study.
Myelin forms a protective sheath around the nerves of the central nervous system, enabling them to transmit electrical impulses that stimulate movement.
In a study published in Developmental Cell, investigators administered a miR-219 mimic to the spinal columns and cerebrospinal fluid of mice with nerve coatings damaged by lysolecithin or by autoimmune encephalomyelitis induced in the animals to model MS.
The findings showed that treatment with miR-219 reinvigorated the function of damaged oligodendrocytes, allowing the myelin to reform and reinsulate the nerves.
MicroRNAs regulate gene expression in cells by acting as molecular silencers, blocking gene expression in certain situations, according to the study. Earlier research points to the absence of miR-219 in the damaged nerves and tissues of neurodegenerative diseases, such as MS.
“We show that miR-2019 targets multiple processes that inhibit myelin formation after nerve injury by the disease process, and that treatment with this microRNA partially restores myelination and limb function,” said lead investigator Richard Q. Lu, PhD. “It is conceivable that augmenting miR-219 treatment with other blockers of myelin regrowth may provide a multipoint treatment strategy for people with demyelinating diseases like MS.”
Although the findings show promise, the authors stress that the work was conducted in laboratory mouse models of MS and that their data cannot be applied to clinical treatment in humans at this time.
In an earlier study, the investigators tested the efficacy and presence of miR-219 in genetically engineered mouse models of MS with chemically induced nerve coating damage by lysolecithin and autoimmune encephalomyelitis. Additionally, the investigators deleted miR-219 in mice to test the impact on myelin-forming oligodendrocyte cells. The results of the study showed that the absence of miR-219 allowed a surge of activity by several inhibitors of nerve remyelination, including the protein Lingo1.
Additional testing demonstrated that miR-2019 is an essential part of the network that targets and blocks molecules that inhibit oligodendrocytes ability to form myelin. The findings from these studies prompted the current study.
The investigators are now attempting to develop additional mimics of miR-219 and therapeutically effective formulations of the microRNA to ease its delivery. They will also continue to test the efficacy of miR-219 treatment in different neurodegenerative diseases.