| Timing of appearance of late oligodendrocyte progenitors coincides with enhanced susceptibility of preterm rabbit cerebral white matter to hypoxia-ischemia. | |
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MedLine Citation:
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PMID: 20068573 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Emerging evidence supports that premature infants are susceptible to both cerebral white and gray matter injury. In a fetal rabbit model of placental insufficiency, preterm rabbits at embryonic day 22 (E22) exhibited histologic evidence of gray matter injury but minimal white matter injury after global hypoxia-ischemia (H-I). We hypothesized that the dissociation between susceptibility to gray and white matter injury at E22 was related to the timing of appearance of late oligodendrocyte progenitors (preOLs) that are particularly vulnerable in preterm human white matter lesions. During normal rabbit oligodendrocyte (OL) lineage progression, early OL progenitors predominated at E22. PreOL density increased between E24 and E25 in major forebrain white matter tracts. After H-I at E22 and E25, we observed a similar magnitude of cerebral H-I, assessed by cortical microvascular blood flow, and gray matter injury, assessed by caspase activation. However, the increased preOL density at E25 was accompanied by a significant increase in acute white matter injury after H-I that coincided with enhanced preOL degeneration. At E29, significant white matter atrophy developed after H-I at E25 but not E22. Thus, the timing of appearance of preOLs coincided with onset of a developmental window of enhanced white but not gray matter susceptibility to H-I. |
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Authors:
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Joshua R Buser; Kristen N Segovia; Justin M Dean; Kerst Nelson; Douglas Beardsley; Xi Gong; Ning Ling Luo; Jennifer Ren; Ying Wan; Art Riddle; Melissa M McClure; Xinhai Ji; Matthew Derrick; A Roger Hohimer; Stephen A Back; Sidhartha Tan |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-01-13 |
Journal Detail:
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Title: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism Volume: 30 ISSN: 1559-7016 ISO Abbreviation: J. Cereb. Blood Flow Metab. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-05-03 Completed Date: 2010-05-27 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 8112566 Medline TA: J Cereb Blood Flow Metab Country: United States |
Other Details:
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Languages: eng Pagination: 1053-65 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239-3098, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Basal Ganglia / cytology, embryology Caspase 3 / metabolism Cell Lineage Cerebral Cortex* / embryology, pathology, physiopathology Female Fetus / pathology, physiopathology Gestational Age Humans Hypoxia-Ischemia, Brain* / pathology, physiopathology Nerve Fibers, Myelinated* / pathology, physiology Oligodendroglia / cytology, physiology* Pregnancy Rabbits Stem Cells / cytology, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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1R01NS043285/NS/NINDS NIH HHS; 1R01NS051402/NS/NINDS NIH HHS; 1R01NS054044/NS/NINDS NIH HHS; K02NS41343/NS/NINDS NIH HHS; R01 NS051402-01A2/NS/NINDS NIH HHS; R01 NS051402-02/NS/NINDS NIH HHS; R01 NS051402-03/NS/NINDS NIH HHS; R01 NS051402-04/NS/NINDS NIH HHS; R37NS045737/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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EC 3.4.22.-/Caspase 3 |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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