Late Oligodendrocyte Progenitors Coincide with the Developmental Window of Vulnerability for Human Perinatal White Matter Injury
By S. Back, N. Luo, Natalya S. Borenstein, J. Levine, Joseph J. Volpe, H. Kinney. Journal of Neuroscience, 2001
928 citations recorded by the source corpus.
Hypoxic-ischemic injury to the periventricular cerebral white matter [periventricular leukomalacia (PVL)] results in cerebral palsy and is the leading cause of brain injury in premature infants. The principal feature of PVL is a chronic disturbance of myelination and suggests that oligodendrocyte (OL) lineage progression is disrupted by ischemic injury. We determined the OL lineage stages at risk for injury during the developmental window of vulnerability for PVL (23–32 weeks, postconceptional age). In 26 normal control autopsy human brains, OL lineage progression was defined in parietal white matter, a region of predilection for PVL. Three successive OL stages, the late OL progenitor, the immature OL, and the mature OL, were characterized between 18 and 41 weeks with anti-NG2 proteoglycan, O4, O1, and anti-myelin basic protein (anti-MBP) antibodies. NG2+O4+ late OL progenitors were the predominant stage throughout the latter half of gestation. Between 18 and 27 weeks, O4+O1+ immature OLs were a minor population (9.9 ± 2.1% of total OLs; n = 9). Between 28 and 41 weeks, an increase in immature OLs to 30.9 ± 2.1% of total OLs (n = 9) was accompanied by a progressive increase in MBP+ myelin sheaths that were restricted to the periventricular white matter. The developmental window of high risk for PVL thus precedes the onset of myelination and identifies the late OL progenitor as the major potential target. Moreover, the decline in incidence of PVL at ∼32 weeks coincides with the onset of myelination in the periventricular white matter and suggests that the risk for PVL is related to the presence of late OL progenitors in the periventricular white matter.
Subfields: Neurology, Pediatrics, Perinatology and Child Health, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/51b7afc5167d7645bcb43a32b4e2a01be8e86d5a
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Citations in the corpus
- Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across species (2013, background): “…at pnd 1–3, is particularly sensitive to damage from HI and metabolic insults, and is likely to result from the specific vulnerability of immature OLs to oxidative stress, NMDA receptor over-stimulation, and the presence of free radicals (Back et al., 2001; Huang et al., 2009a; Johnston, 1995).”
- Selective Vulnerability of Late Oligodendrocyte Progenitors to Hypoxia–Ischemia (2002, methodology): “We focused on the susceptibility of the late OL progenitor, because this OL stage predominates throughout the high-risk period for PVL (Back et al., 2001).”
- Neurobiology of Periventricular Leukomalacia in the Premature Infant (2001, background): “Our studies identified the dominant form of OL in the WM of the human premature infant, and perhaps therefore the key cellular target in PVL, as an early differentiating OL with the specific immunocytochemical characteristics of an OL precursor (44).”
- Normal Development of Brain Circuits (2010, background): “Premyelinating oligodendrocytes may be particularly sensitive to perinatal hypoxia or ischemia, which may disrupt white matter tracts in the frontal and temporal lobe to produce cerebral palsy or mental retardation (Back et al, 2001; Ness et al, 2001).”
- The Toll-Like Receptor TLR4 Is Necessary for Lipopolysaccharide-Induced Oligodendrocyte Injury in the CNS (2002, background): “mediates injury to oligodendroglial precursors, the cell type injured in human PVL (Back et al., 2001; Volpe, 2001).”