Researchers recently reported identifying a small protein that may be targeted to promote repair of damaged tissue associated with multiple sclerosis. The molecule, Endothelin-1 (ET-1), is shown to inhibit repair of myelin. Myelin damage is a hallmark characteristic of MS. The study from the Center for Neuroscience Research at Children’s National Health System demonstrates that blocking ET-1 pharmacologically or using a genetic approach could promote myelin repair.
The brain produces new cells to repair the damage from MS years after symptoms appear. However, in most cases the cells are unable to complete the repair, as unknown factors limit this process. In MS patients, brain inflammation in random patches, or lesions, leads to destruction of myelin, the fatty covering that insulates nerve cell fibers called axons in the brain, and aids in transmission of signals to other neurons.
Repair of damaged MS plaques is carried out by endogenous oliogdendrocytle progenitor cells (OPCs) in a process called remyelination. Current MS therapy can be effective in patients with relapsing and remitting MS, but “have little impact in promoting remyelination in tissue,” the researchers stated. Several studies have shown that OPCs fail to differentiate in chronic MS lesions.
Targeting ET-1 is a process that involves identifying signals in cells that could promote lesion repair. “We demonstrate that ET-1 drastically reduces the rate of remyelination,” says Vittorio Gallo, PhD, director of the center . As such, ET-1 is “potentially a therapeutic target to promote lesion repair in deymyelinated tissue.” It could play a “crucial role in preventing normal myelination in MS and in other demyelinating diseases,” Gallo said.
The study was published in the journal Neuron.