IL-1β induces hypomyelination in the periventricular white matter through inhibition of oligodendrocyte progenitor cell maturation via FYN/MEK/ERK signaling pathway in septic neonatal rats

Glia ◽  
2015 ◽  
Vol 64 (4) ◽  
pp. 583-602 ◽  
Author(s):  
Di Xie ◽  
Fengcai Shen ◽  
Shaoru He ◽  
Mengmeng Chen ◽  
Qianpeng Han ◽  
...  
Keyword(s):  
White Matter ◽  
Signaling Pathway ◽  
Progenitor Cell ◽  
Erk Signaling ◽  
Cell Maturation ◽  
Periventricular White Matter ◽  
Neonatal Rats ◽  
Oligodendrocyte Progenitor Cell ◽  
Oligodendrocyte Progenitor

scholarly journals Regulation of Oligodendrocyte Progenitor Cell Maturation by PPARδ: Effects on Bone Morphogenetic Proteins

ASN NEURO ◽  
2010 ◽  
Vol 2 (1) ◽  
pp. AN20090033 ◽  
Author(s):  
Maria Vittoria Simonini ◽  
Paul E Polak ◽  
Anne I Boullerne ◽  
Jeffrey M Peters ◽  
Jill C Richardson ◽  
...  
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Progenitor Cell ◽  
Cell Maturation ◽  
Oligodendrocyte Progenitor Cell ◽  
Oligodendrocyte Progenitor

Oligodendrocyte Progenitor Cell Proliferation and Fate after White Matter Stroke in Juvenile and Adult Mice

2018 ◽  
Vol 40 (5-6) ◽  
pp. 601-616 ◽  
Author(s):  
Andra L. Dingman ◽  
Krista M. Rodgers ◽  
Robert M. Dietz ◽  
Sean P. Hickey ◽  
Alexandra P. Frazier ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
White Matter ◽  
Cell Fate ◽  
Cellular Response ◽  
Progenitor Cell ◽  
Ischemic Injury ◽  
Oligodendrocyte Progenitor Cell ◽  
Oligodendrocyte Progenitor ◽  
Time Points ◽  
Adult Mice

The incidence of stroke in children is 2.4 per 100,000 person-years and results in long-term motor and cognitive disability. In ischemic stroke, white matter (WM) is frequently injured, but is relatively understudied compared to grey matter injury. Previous research suggests that the cellular response to WM ischemic injury is different at different ages. Little is known about whether WM repair mechanisms differ in children and adults. We utilized a model of focal ischemic WM injury to determine the oligodendrocyte (OL) response to focal WM ischemic injury in juvenile and adult mice. Methods: Juvenile (21–25 days of age) versus adult (2–3 months of age) mice underwent stereotaxic injection of the potent vasoconstrictor N5-(1-iminoethyhl)-L-ornithine (L-NIO) into the lateral corpus callosum (CC). Animals were sacrificed on postoperative day 3 (acute) or 21 (chronic). Cell birth-dating was performed acutely after WM stroke with 5-ethynyl-2-deoxyuridine (EdU) injected intraperitoneally. Immunohistochemistry was performed, as well as stereology, to measure injury volume. The acute oligodendrocyte progenitor cell (OPC) proliferation and the chronic OL cell fate were determined with immunohistochemistry. Compound action potentials were measured in the CC at acute and chronic time points. Results: Acutely WM injury volume was smaller in juveniles. There was significantly greater OPC proliferation in juvenile animals (acute) compared to adults, but newly born OLs did not survive and mature into myelinating cells at chronic time points. In addition, juveniles did not have improved histological or functional recovery when compared to adults. Protecting newly born OPCs is a potential therapeutic target in children with ischemic stroke.

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