TY - JOUR
T1 - Coordinated control of oligodendrocyte development by extrinsic and intrinsic signaling cues
AU - He, Li
AU - Lu, Q. Richard
N1 - Funding Information:
We thank Yu Yang for critical reading. Due to space limitations, we apologize to those whose work was not discussed. This review was supported in part by grants from the US National Institutes of Health (R01NS072427 and R01NS075243) and the National Multiple Sclerosis Society (RG4568).
PY - 2013/4
Y1 - 2013/4
N2 - Oligodendrocytes, the myelin-forming cells for axon ensheathment in the central nervous system, are critical for maximizing and maintaining the conduction velocity of nerve impulses and proper brain function. Demyelination caused by injury or disease together with failure of myelin regeneration disrupts the rapid propagation of action potentials along nerve fibers, and is associated with acquired and inherited disorders, including devastating multiple sclerosis and leukodystrophies. The molecular mechanisms of oligodendrocyte myelination and remyelination remain poorly understood. Recently, a series of signaling pathways including Shh, Notch, BMP and Wnt signaling and their intracellular effectors such as Olig1/2, Hes1/5, Smads and TCFs, have been shown to play important roles in regulating oligodendrocyte development and myelination. In this review, we summarize our recent understanding of how these signaling pathways modulate the progression of oligodendrocyte specification and differentiation in a spatiotemporally-specific manner. A better understanding of the complex but coordinated function of extracellular signals and intracellular determinants during oligodendrocyte development will help to devise effective strategies to promote myelin repair for patients with demyelinating diseases.
AB - Oligodendrocytes, the myelin-forming cells for axon ensheathment in the central nervous system, are critical for maximizing and maintaining the conduction velocity of nerve impulses and proper brain function. Demyelination caused by injury or disease together with failure of myelin regeneration disrupts the rapid propagation of action potentials along nerve fibers, and is associated with acquired and inherited disorders, including devastating multiple sclerosis and leukodystrophies. The molecular mechanisms of oligodendrocyte myelination and remyelination remain poorly understood. Recently, a series of signaling pathways including Shh, Notch, BMP and Wnt signaling and their intracellular effectors such as Olig1/2, Hes1/5, Smads and TCFs, have been shown to play important roles in regulating oligodendrocyte development and myelination. In this review, we summarize our recent understanding of how these signaling pathways modulate the progression of oligodendrocyte specification and differentiation in a spatiotemporally-specific manner. A better understanding of the complex but coordinated function of extracellular signals and intracellular determinants during oligodendrocyte development will help to devise effective strategies to promote myelin repair for patients with demyelinating diseases.
KW - HDAC
KW - Shh, BMP, Notch and Wnt signaling
KW - chromatin remodeling factors
KW - differentiation
KW - miRNAs
KW - myelination
KW - oligodendrocyte
KW - specification
KW - transcription factors
UR - http://www.scopus.com/inward/record.url?scp=84877873616&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84877873616&partnerID=8YFLogxK
U2 - 10.1007/s12264-013-1318-y
DO - 10.1007/s12264-013-1318-y
M3 - Review article
C2 - 23494530
AN - SCOPUS:84877873616
SN - 1673-7067
VL - 29
SP - 129
EP - 143
JO - Neuroscience Bulletin
JF - Neuroscience Bulletin
IS - 2
ER -