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Stem Cell Research Inflammation

Stem Cell Research Reveals Culprit Of Remyelination

5 months ago

3036  0
Posted on Dec 21, 2018, 9 p.m.

The spontaneous regeneration of brain fatty insulators that keep neurons communicating is called remyelination; stem cell research has revealed the culprit of what prevents remyelination and possibly leads to multiple sclerosis and other inflammatory diseases.

Scientists from the University of Buffalo have revealed preclinical findings showing activation of a specific transcription factor, PRRX1 in human oligodendrocyte progenitor cells, can induce pathological quiescence in adult stem cells, which is when adult stem cells are rendered incapable of responding to injury by producing myelin-forming oligodendrocytes; failure to remyelinate is the key feature of multiple sclerosis, as published in Cell Reports.

MS research primarily focuses on drugs that induce differentiation of human oligodendrocyte progenitors, the study presents a novel concept based on blocking the pathological quiescence of progenitors. Switching the gene on was found to cause problems in myelin repair by blocking proliferation of oligodendrocyte cells, which are the stem cell like precursors responsible for all myelin regeneration in the adult brain.

PRRX1 expression resulted in cell cycle arrest and quiescence of oligodendrocyte progenitors that disabled production of myelin; quiescence induced by PRRX1 prevented cell colonization of white matter and effective myelin regeneration by transplanted human oligodendrocyte progenitors in animal models of leukodystrophy; blocking expression of this transcript was found to prevent negative effects of proinflammatory cytokines such as interferon-y which regulates its expression.

Findings suggest new targets for therapeutic intervention, and how the disease environment in multiple sclerosis may prevent effective myelin repair and regeneration; finding pathological quiescence is key to inability to repair and regenerate myelin provides a novel direction for research, which the team plans to further pursue in hope of identifying possible treatments that may work by overcoming pathological quiescence of oligodendrocyte precursors in demyelinating lesions which characterize multiple sclerosis.

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