{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:38:46Z","timestamp":1791938326580,"version":"4.3.4"},"reference-count":40,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,4,4]],"date-time":"2008-04-04T00:00:00Z","timestamp":1207267200000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2008,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Abnormal myelination is a major pathological sequela of chronic periventricular white matter injury in survivors of premature birth. We tested the hypothesis that myelination failure in chronic hypoxia\u2010ischemia\u2010induced periventricular white matter injury is related to persistent depletion of the oligodendrocyte (OL) precursor pool required to generate mature myelinating OLs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A neonatal rat model of hypoxia\u2010ischemia was used where acute degeneration of late OL progenitors (preOLs) occurs via a mostly caspase\u2010independent mechanism. The fate of OL lineage cells in chronic cerebral lesions was defined with OL lineage\u2010specific markers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Acute caspase\u20103\u2010independent preOL degeneration from hypoxia\u2010ischemia was significantly augmented by delayed preOL death that was caspase\u20103\u2010dependent. Degeneration of preOLs was offset by a robust regenerative response that resulted in a several\u2010fold expansion in the pool of surviving preOLs in chronic lesions. However, these preOLs displayed persistent maturation arrest with failure to differentiate and generate myelin. When preOL\u2010rich chronic lesions sustained recurrent hypoxia\u2010ischemia at a time in development when white matter is normally resistant to injury, an approximately 10\u2010fold increase in caspase\u2010dependent preOL degeneration occurred relative to lesions caused by a single episode of hypoxia\u2010ischemia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>The mechanism of myelination failure in chronic white matter lesions is related to a combination of delayed preOL degeneration and preOL maturation arrest. The persistence of a susceptible population of preOLs renders chronic white matter lesions markedly more vulnerable to recurrent hypoxia\u2010ischemia. These data suggest that preOL maturation arrest may predispose to more severe white matter injury in preterm survivors that sustain recurrent hypoxia\u2010ischemia. Ann Neurol 2008<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.21359","type":"journal-article","created":{"date-parts":[[2008,4,4]],"date-time":"2008-04-04T10:58:45Z","timestamp":1207306725000},"page":"520-530","source":"Crossref","is-referenced-by-count":306,"title":["Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury"],"prefix":"10.1002","volume":"63","author":[{"given":"Kristen N.","family":"Segovia","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa","family":"McClure","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew","family":"Moravec","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning 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