Pro-inflammatory signaling molecules which have been involved in plates sclerosis (MS) cause problems of growth and development of myelin manufacturing cells in the brain, according to a study carried out in cell models.
The results may have implications for the treatment of MS, as promoting the growth of myelin manufacturing cells could be a strategy of therapeutic approaches, researchers said.
The study, “Pro-inflammatory molecules involved in multiple sclerosis divert the development of lines of lineage of human human oligodes“, Was published in Neuroimmunology and neuroinflammation neurology.
Myelin is a fatty substance that wraps around the nerve fibers and helps them send electrical signals, operating such as rubber insulation around a metal wire. In MS, inflammation in the brain and spinal cord causes myelin damage, which causes neurological signaling problems that ultimately cause symptoms of illness.
In the brain, myelin is made mainly by specialized cells called oligodendrocytes. When the myelin is damaged, the oligodendrocytes can normally go into action to do new myelin and repair the damage. In MS, the repair activity of the myelin of these cells is altered. The biological mechanisms that make dysfunctional oligodendrocytes in the MS are not entirely understood.
Examine the signaling molecules
A team led by scientists from Canada has led a series of experiences to see how certain inflammatory signaling molecules affect the growth of oligodendrocytes (OPC), immature cells capable of developing in myelin manufacturing oligodendrocytes.
The researchers studied the effects of the factor of alpha tumor necrosis (TNF-alpha) and the interferon gamma, which are both pro-inflammatory signaling molecules which have proven to play a role in the inflammation of the driving of MS.
“These (inflammatory signaling molecules), among others, prove to be increasing in the famous liquid and the peripheral blood of people with MS,” wrote scientists.
The researchers found that these two inflammatory signaling molecules are not cytotoxic to OPCs. In other words, they don’t kill immature cells. But exposure to one or the other of the two inflammatory molecules made OPCs less effective in developing in mature oligodetrocytes and manufacturing myelin.
Researchers noted that OPCs exposed to TNF-Alpha tend to take the characteristics of astrocytes, a separate brain cell type that helps support the nervous function but is not equipped to make and effectively repair myelin.
“Rather than differentiating themselves in (myelin manufacturing oligodendrocyes), OPCs can rather give birth to astrocytes, contributing to the failure of a good repair of myelin,” they wrote.
Although the main experiments have been carried out using cellular models, researchers have found astrocyte -type OPCs in damaged cerebral tissues with PES, which implies that this mechanism can also occur in people with disease.
“The identification of this OPC population with a signature of an astrocyte gene located within the brain lesions of human MS can prove to be a new mechanism preventing adequate remediation in an inflammatory context,” wrote scientists.
The results indicate “a potential therapeutic avenue – strategies aimed at promoting OPC differentiation along the line (oligodendrocye) while inhibiting astrocyte conversion could improve remyling and mitigate the progression of the disease,” concluded the team.
