Progress in Periventricular Leukomalacia

Deng, Wenbin; Pleasure, Jeanette R.; Pleasure, David E

doi:10.1001/archneur.65.10.1291

Cited by 151 publications

(108 citation statements)

References 35 publications

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“…PVL is the most important brain pathology underlying cerebral palsy in premature infants. No specific therapy for PVL presently exists, in part because the pathogenesis has not been well understood 1,2 .…”

Section: Discussionmentioning

confidence: 99%

Mouse Models of Periventricular Leukomalacia

Shen¹,

Plane²,

Deng³

2010

JoVE

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We describe a protocol for establishing mouse models of periventricular leukomalacia (PVL). PVL is the predominant form of brain injury in premature infants and the most common antecedent of cerebral palsy. PVL is characterized by periventricular white matter damage with prominent oligodendroglial injury. Hypoxia/ischemia with or without systemic infection/inflammation are the primary causes of PVL. We use P6 mice to create models of neonatal brain injury by the induction of hypoxia/ischemia with or without systemic infection/inflammation with unilateral carotid ligation followed by exposure to hypoxia with or without injection of the endotoxin lipopolysaccharide (LPS). Immunohistochemistry of myelin basic protein (MBP) or O1 and electron microscopic examination show prominent myelin loss in cerebral white matter with additional damage to the hippocampus and thalamus. Establishment of mouse models of PVL will greatly facilitate the study of disease pathogenesis using available transgenic mouse strains, conduction of drug trials in a relatively high throughput manner to identify candidate therapeutic agents, and testing of stem cell transplantation using immunodeficiency mouse strains. Video LinkThe video component of this article can be found at http://www.jove.com/video/1951/ ProtocolDetailed procedures of creating neonatal brain injury in P6 mice:1. Postnatal day 6 (P6) mice are anesthetized with indirect cooling on ice to the point of unresponsiveness to noxious stimulation (deep anesthesia). 2. Following cleaning the skin with alcohol, a midline ventral incision is made in the anterior neck. 3. Under a dissecting microscope, the bifurcation of the right common carotid artery is approached by gently retracting the omohyoid and sternocleidomastoid muscles. 4. The fascia around the carotid sheath is removed, and the proximal internal branch isolated from the nearby vagus nerve and sympathetic ganglia with a hook. The internal carotid artery is then cauterized using a cauterizing tip. 5. Following cauterization, the skin incision is sutured, and the animal is kept warm until fully awake and then returned to the dam. 6. One hour after ligation, the animal is placed in a sealed chamber infused with nitrogen until a level of 6.0% O 2 is reached. The animal is then exposed to 35 min of hypoxia. 7. After hypoxia exposure, the mouse recovers on a heating pad (33°C) for 30 min and then is returned to the dam. For creation of brain injury with combined hypoxia/ischemia and infection/inflammation, the animal is then injected intraperitoneally with 0.015 ml of lipopolysaccharide (LPS, 1 mg/kg). 8. Four days post-hypoxia/ischemia, mice are anesthetized with indirect cooling on ice to the point of unresponsiveness to noxious stimuli, then perfused with saline and then 4% paraformaldehyde. Brains are removed and cryoprotected.

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Section: Discussionmentioning

confidence: 99%

Mouse Models of Periventricular Leukomalacia

Shen¹,

Plane²,

Deng³

2010

JoVE

Self Cite

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“…Previously published references were consulted concerning the diagnostic suggestions for periventricular-intraventricular hemorrhage and PVL in premature infants and the grading criteria for PVL (Deng et al, 2008).…”

Section: Pvl Diagnosis and Grading Standardsmentioning

confidence: 99%

Relation between prognosis and changes of MBP and S100B in premature infants with periventricular leukomalacia

Huang¹,

Zhang²,

Zhang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. This study aims to explore the relation between changes in myelin basic protein (MBP) and S100 protein (S100B) serum levels and prognosis in premature infants with periventricular leukomalacia (PVL). In our hospital, 78 premature infants with PVL and 43 normal premature infants were studied from July 1, 2007 to December 31, 2008. MBP and S100B serum levels were detected at 1, 3, 7, and 14 days after birth by using enzyme-linked immunosorbent assay. All infants were followed four times (once every 3 months) after discharge from hospital. Their intelligence quotient and physical development index were tested by using Gesell developmental scales. The MBP serum levels were significantly higher in premature infants with PVL at any time point than in normal premature infants. S100B serum levels gradually increased at 1, 3, and 7 days; peaked on the 7th day; and then gradually decreased to the normal level on the 14th day. The intelligence quatient and physical development index of infants with increased S100B and MBP levels on the 7th day were lower than those of infants who had normal S100B and MBP levels and those of normal premature infants. A negative relation exists between S100B and MBP 4339 MBP and S100B in premature infants ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 4338-4343 (2015) serum levels and prognosis in PVL infants. An increase of MBP and S100B levels lasting >7 days could cause poor prognosis.

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“…As is well known, the periventricular leukomalacia is characterized by injury of myelinated nerve fibers mostly of the corpus callosum [19]. Therefore, in our study the immunohistochemical analysis of oligodendrocytes in organotypic brain slices culture in the zone of lateral ventricles with corpus callosum was carried out.…”

Section: Discussionmentioning

confidence: 97%

Untitled

2017

Fiziol Zh

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Multipotent mesenchymal stromal cells (MMSCs) demonstrated a measurable therapeutic effect following transplantation into animal models of periventricular leukomalacia (PVL), brain white-matter degeneration for PVL model in vitro (PVLmiv) subjecting cultures to oxygen-glucose deprivation (OGD) and endotoxin lipopolysaccharide (LPS). This approach allowed us to simulate important pathogenic factors both responsible for PVL, hypoxic-ischemic component and inflammation. Based on the cell viability and the glial reaction, we evaluated distant effects of MMSCs on brain slices with PVLmiv in the non-contact co-culture. Cell viability was assessed by the measurement of cytoplasmic enzyme lactate dehydrogenase (LDH) released into the culture medium. Glial reaction in the periventricular regions of slices was analyzed immunochistochemically using specific antibodies to glial markers of oligodendrocytes, astrocytes and microglia (Rip, respectively

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Progress in Periventricular Leukomalacia

Cited by 151 publications

References 35 publications

Mouse Models of Periventricular Leukomalacia

Mouse Models of Periventricular Leukomalacia

Relation between prognosis and changes of MBP and S100B in premature infants with periventricular leukomalacia

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