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Versican and brevican are expressed with distinct pathology in neonatal hypoxic‐ischemic injury
Author(s) -
Leonardo Christopher C.,
Eakin Autumn K.,
Ajmo Joanne M.,
Gottschall Paul E.
Publication year - 2008
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21553
Subject(s) - versican , external capsule , white matter , pathology , lesion , glial fibrillary acidic protein , biology , hippocampal formation , cresyl violet , corpus callosum , microglia , internal capsule , immunohistochemistry , anatomy , medicine , endocrinology , immunology , staining , inflammation , magnetic resonance imaging , cartilage , radiology , proteoglycan
The developing brain is uniquely susceptible to injury after exposure to hypoxia‐ischemia (H‐I). Lecticans are developmentally regulated in formative white matter and exert growth‐inhibitory effects in several adult injury models, yet little is known regarding their role in neonatal H‐I injury. The main objectives of this study were to examine the expression profiles of brevican and versican in rat using a standard H‐I model and to determine whether altered expression was associated with distinct components of white and gray matter pathology. The H‐I procedure in postnatal day 7 rats produced progressive injury limited to the ipsilateral hemisphere. Cresyl violet staining revealed severe cavitary infarctions at 14 and 21 days that were absent at 4 days. Cellular damage, as measured by glial fibrillary acidic protein and fractin immunoreactivity, occurred in cortical and subcortical gray matter at all end points. O4 sulfatide immunoreactivity was reduced in the external capsule, hippocampal fimbria, and corpus striatum at 4 days relative to that contralaterally, suggesting the loss of preoligodendrocytes. Brevican expression was reduced in the cortex and hippocampus at 4 days but was markedly elevated at later end points, localizing to regions of cellular damage both in and proximal to the lesion core. However, versican was reduced in the external capsule 4 days after H‐I, a reduction that was sustained up to 21 days in white matter. These data demonstrate unique expression profiles for lecticans after neonatal H‐I, suggesting brevican deposition is elevated in response to progressive gray matter injury, whereas diminished versican expression may be associated with deep cerebral white matter injury. © 2007 Wiley‐Liss, Inc.