The effect of hypoxic-ischemic brain injury in perinatal rats on the abundance and proteolysis of brevican and NG2
| Autor: | Paul E. Gottschall, John D. Sandy, Margaret Anello, Barbara G. Muffly, Joanne Mayer, Autumn K. Eakin, James Aya-ay |
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| Rok vydání: | 2004 |
| Předmět: |
medicine.medical_specialty
Time Factors Ischemia Nerve Tissue Proteins Hippocampal formation Biology Hippocampus chemistry.chemical_compound Developmental Neuroscience Internal medicine medicine Animals Lectins C-Type Antigens Brevican Microglia medicine.disease Oligodendrocyte Rats medicine.anatomical_structure Endocrinology nervous system Neurology chemistry Animals Newborn Chondroitin Sulfate Proteoglycans Chondroitin sulfate proteoglycan Cerebral cortex Hypoxia-Ischemia Brain Proteoglycans Neuroscience Astrocyte Peptide Hydrolases |
| Zdroj: | Experimental neurology. 193(1) |
| ISSN: | 0014-4886 |
| Popis: | Oligodendrocyte (OL) progenitor cells are particularly susceptible to perinatal hypoxia/ischemia (H–I) resulting in decreased myelination and attenuated development of white matter fiber tracts. Brevican is an aggregating chondroitin sulfate proteoglycan (CSPG) secreted by OLs and their progenitors prior to and during active developmental myelination whereas neuron-glia antigen 2 (NG2) is a transmembrane CSPG produced by early OL progenitors. Although both proteoglycans are associated with maturation of OLs, it is not known if they are altered by H–I brain injury in the neonate. We have therefore examined the time course of changes in brevican and NG2 abundance and proteolysis in the neonatal rat hippocampus after H–I. In a standard H–I model of unilateral carotid artery ligation and exposure to hypoxia, a cavitary infarct involving the ipsilateral parietal and temporal regions of cerebral cortex, hippocampus, and striatum of most rat pups was clearly evident 4 days after H–I. The abundance of total extractable brevican was markedly reduced in the ipsilateral hippocampus at 1 and 14 days after H–I (relative to the contralateral side). At these times, the total G1 proteolytic fragment of brevican was lower in the ipsilateral hippocampus and the level of a protease-generated brevican fragment was significantly diminished in the OL-rich hippocampal fimbria. Hippocampal NG2 levels were also lower at 1 and 4 days after H–I, but were not different from the contralateral side at 14 days. Since brevican, brevican G1 fragment, and NG2 loss occur around the time of progressive cell death and the appearance of the infarct, it may be that H–I rapidly induces a cellular response that actively depletes these proteoglycans from the hippocampal matrix. While the mechanism of this loss is unclear, it would appear to be an early event in the process that could be involved in apoptotic cell death and/or tissue injury. |
| Databáze: | OpenAIRE |
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