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Laminin regulates oligodendrocyte development and myelination
Funding information: National Heart, Lung, and Blood Institute, Grant/Award Number: R01HL146574; National Institute on Aging, Grant/Award Numbers: R21AG064422, R21AG073862, RF1AG065345
Abstract
Oligodendrocytes are the cells that myelinate axons and
provide trophic support to neurons in the CNS. Their dysfunction has
been associated with a group of disorders known as demyelinating
diseases, such as multiple sclerosis. Oligodendrocytes are derived from
oligodendrocyte precursor cells, which differentiate into premyelinating
oligodendrocytes and eventually mature oligodendrocytes. The
development and function of oligodendrocytes are tightly regulated by a
variety of molecules, including laminin, a major protein of the
extracellular matrix. Accumulating evidence suggests that laminin
actively regulates every aspect of oligodendrocyte biology, including
survival, migration, proliferation, differentiation, and myelination.
How can laminin exert such diverse functions in oligodendrocytes? It is
speculated that the distinct laminin isoforms, laminin receptors, and/or
key signaling molecules expressed in oligodendrocytes at different
developmental stages are the reasons. Understanding molecular targets
and signaling pathways unique to each aspect of oligodendrocyte biology
will enable more accurate manipulation of oligodendrocyte development
and function, which may have implications in the therapies of
demyelinating diseases. Here in this review, we first introduce
oligodendrocyte biology, followed by the expression of laminin and
laminin receptors in oligodendrocytes and other CNS cells. Next, the
functions of laminin in oligodendrocyte biology, including survival,
migration, proliferation, differentiation, and myelination, are
discussed in detail. Last, key questions and challenges in the field are
discussed. By providing a comprehensive review on laminin's roles in OL
lineage cells, we hope to stimulate novel hypotheses and encourage new
research in the field.
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