Erythropoietin signaling promotes oligodendrocyte development following prenatal systemic hypoxic-ischemic brain injury.
Erythropoietin signaling promotes oligodendrocyte development following prenatal systemic hypoxic-ischemic brain injury.
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DOI:
10.1038/pr.2013.155
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发表时间:
2013-12
影响因子:
3.6
通讯作者:
Robinson, Shenandoah
中科院分区:
文献类型:
--
作者:
Jantzie, Lauren L.;Miller, Robert H.;Robinson, Shenandoah
Brain injury from preterm birth causes white matter injury (WMI), and leads to chronic neurological deficits including cerebral palsy, epilepsy, cognitive and behavioral delay. Immature O4+ oligodendrocytes are particularly vulnerable to WMI. Understanding how the developing brain recovers after injury is essential to finding more effective therapeutic strategies. Erythropoietin (EPO) promotes neuronal recovery after injury however its role in enhancing oligodendroglial lineage recovery is unclear. Previously we found recombinant EPO (rEPO)-treatment enhances MBP expression and functional recovery in adult rats after prenatal transient systemic hypoxia-ischemia (TSHI). We hypothesized that after injury rEPO would enhance oligodendroglial lineage cell genesis, survival, maturation and myelination. In vitro assays were used to define how rEPO contributes to specific stages of oligodendrocyte development and recovery after TSHI. After prenatal TSHI injury, rEPO promotes genesis of oligodendrocyte progenitors from oligodendrospheres, survival of oligodendrocyte precursor cells (OPCs) and O4+ immature oligodendrocytes, O4+ cell process extension and MBP expression. rEPO did not alter OPC proliferation. Together, these studies demonstrate that EPO signaling promotes critical stages of oligodendroglial lineage development and recovery after prenatal TSHI injury. Erythropoietin treatment may be beneficial to preterm and other infant patient populations with developmental brain injury hallmarked by WMI.
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DOI:
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发表时间:
2012-07
影响因子:
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作者:
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期刊:
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影响因子:
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影响因子:
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