Arrested preoligodendrocyte maturation contributes to myelination failure in premature infants

被引：371

作者：

Buser, Joshua R. ^{[1
]}

Maire, Jennifer ^{[1
]}

Riddle, Art ^{[1
]}

Gong, Xi ^{[1
]}

Thuan Nguyen ^{[2
]}

Nelson, Kerst ^{[1
]}

Luo, Ning Ling ^{[1
]}

Ren, Jennifer ^{[1
]}

Struve, Jaime ^{[3
]}

Sherman, Larry S. ^{[3
]}

Miller, Steven P. ^{[4
]}

Chau, Vann ^{[4
]}

Hendson, Glenda ^{[5
]}

Ballabh, Praveen ^{[6
,7
]}

Grafe, Marjorie R. ^{[8
,9
]}

Back, Stephen A. ^{[1
,10
]}

机构：

[1] Oregon Hlth & Sci Univ, Dept Pediat, Portland, OR 97239 USA

[2] Oregon Hlth & Sci Univ, Dept Prevent Med, Portland, OR 97239 USA

[3] Oregon Natl Primate Res Ctr, Div Neurosci, Hillsboro, OR USA

[4] Univ British Columbia, Dept Pediat, Vancouver, BC V6T 1W5, Canada

[5] Univ British Columbia, Dept Pathol, Vancouver, BC V6T 1W5, Canada

[6] New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA

[7] New York Med Coll, Dept Anat & Cell Biol, Valhalla, NY 10595 USA

[8] Oregon Hlth & Sci Univ, Dept Publ Hlth, Portland, OR 97239 USA

[9] Oregon Hlth & Sci Univ, Dept Pathol, Portland, OR 97239 USA

[10] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA

来源：

ANNALS OF NEUROLOGY | 2012年 / 71卷 / 01期

基金：

加拿大健康研究院;

关键词：

LATE OLIGODENDROCYTE PROGENITORS; CEREBRAL WHITE-MATTER; PERIVENTRICULAR LEUKOMALACIA; BRAIN-INJURY; SELECTIVE VULNERABILITY; EXPRESSION; DIFFERENTIATION; ACTIVATION; MICROGLIA; SCLEROSIS;

D O I：

10.1002/ana.22627

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Objective: The major form of magnetic resonance imagingdefined white matter injury (WMI) comprises diffuse lesions where the burden of small necrotic foci (microscopic necrosis) is poorly defined. We hypothesized that myelination failure associated with diffuse WMI involves an aberrant injury response linked to arrested preoligodendrocyte (preOL) maturation in reactive astrocyte-rich lesions. Methods: A retrospective autopsy series (1983-2000) was selected for cases with diffuse WMI and analyzed relative to prospectively collected contemporary cases (2003-2010). Controls were age-and region-matched to address regional variation in preOL maturation. Successive oligodendrocyte stages were analyzed with lineage-specific markers. Microscopic necrosis was quantified with microglial markers. Axon injury markers defined the burden of axonopathy. Extracellular matrix remodeling was defined by detection of hyaluronic acid (HA), an inhibitor of preOL maturation, and the HA receptor, CD44. Results: In the contemporary case series, diffuse WMI was accompanied by a significant reduction in the burden of microscopic necrosis and axonopathy. Diffuse astrogliosis extended into the lesion surround with elevated HA and astrocyte-expressed CD44. The total population of OL lineage stages was significantly increased in lesions. This increase coincided with significant expansion of the preOL pool. Interpretation: Although these data confirm that microscopic necrosis occurs in contemporary cases, the markedly decreased burden supports that it does not contribute substantially to myelination failure. The primary mechanism of myelination failure involves a disrupted cellular response whereby preOLs fail to differentiate in diffuse astrogliotic lesions. PreOL maturation arrest converts chronic WMI to a more immature state related to the burden of astrogliosis. ANN NEUROL 2012; 71: 93-109

引用

页码：93 / 109

页数：17

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