Perinatal Hypoxia-Ischemia Induces Apoptotic and Excitotoxic Death of Periventricular White Matter Oligodendrocyte Progenitors

2001 ◽  
Vol 23 (3) ◽  
pp. 203-208 ◽  
Author(s):  
Jennifer K. Ness ◽  
Michael J. Romanko ◽  
Raymond P. Rothstein ◽  
Teresa L. Wood ◽  
Steven W. Levison
Keyword(s):  
White Matter ◽  
Periventricular White Matter ◽  
Perinatal Hypoxia ◽  
Oligodendrocyte Progenitors ◽  
Hypoxia Ischemia

scholarly journals Immediate remote ischemic postconditioning after hypoxia ischemia in piglets protects cerebral white matter but not grey matter

2015 ◽  
Vol 36 (8) ◽  
pp. 1396-1411 ◽  
Author(s):  
Mojgan Ezzati ◽  
Alan Bainbridge ◽  
Kevin D Broad ◽  
Go Kawano ◽  
Aaron Oliver-Taylor ◽  
...  
Keyword(s):  
White Matter ◽  
Corpus Callosum ◽  
Grey Matter ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
White Female ◽  
Resonance Spectroscopy ◽  
Periventricular White Matter ◽  
Remote Ischemic Postconditioning ◽  
Hypoxia Ischemia

Remote ischemic postconditioning (RIPostC) is a promising therapeutic intervention whereby brief episodes of ischemia/reperfusion of one organ (limb) mitigate damage in another organ (brain) that has experienced severe hypoxia-ischemia. Our aim was to assess whether RIPostC is protective following cerebral hypoxia-ischemia in a piglet model of neonatal encephalopathy (NE) using magnetic resonance spectroscopy (MRS) biomarkers and immunohistochemistry. After hypoxia-ischemia (HI), 16 Large White female newborn piglets were randomized to: (i) no intervention ( n = 8); (ii) RIPostC – with four, 10-min cycles of bilateral lower limb ischemia/reperfusion immediately after HI ( n = 8). RIPostC reduced the hypoxic-ischemic-induced increase in white matter proton MRS lactate/N acetyl aspartate ( p = 0.005) and increased whole brain phosphorus-31 MRS ATP ( p = 0.039) over the 48 h after HI. Cell death was reduced with RIPostC in the periventricular white matter ( p = 0.03), internal capsule ( p = 0.002) and corpus callosum ( p = 0.021); there was reduced microglial activation in corpus callosum ( p = 0.001) and more surviving oligodendrocytes in corpus callosum ( p = 0.029) and periventricular white matter ( p = 0.001). Changes in gene expression were detected in the white matter at 48 h, including KATP channel and endothelin A receptor. Immediate RIPostC is a potentially safe and promising brain protective therapy for babies with NE with protection in white but not grey matter.

Impact of Xenon on CLIC4 and Bcl-2 Expression in Lipopolysaccharide and Hypoxia-Ischemia-Induced Periventricular White Matter Damage

Neonatology ◽  
2018 ◽  
Vol 113 (4) ◽  
pp. 339-346 ◽  
Author(s):  
Xiangyun Yin ◽  
Jixiu Zhao ◽  
Hong Jiang ◽  
Liangliang Li ◽  
Jian Jiang ◽  
...  
Keyword(s):  
White Matter ◽  
Periventricular White Matter ◽  
White Matter Damage ◽  
Hypoxia Ischemia

Alteration in rectification of potassium channels in perinatal hypoxia ischemia brain damage

2015 ◽  
Vol 113 (2) ◽  
pp. 592-600 ◽  
Author(s):  
Penghui Chen ◽  
Liyan Wang ◽  
Qiyue Deng ◽  
Huaizhen Ruan ◽  
Wenqin Cai
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Brain Damage ◽  
Lucifer Yellow ◽  
Membrane Resistance ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
High Signal ◽  
Perinatal Hypoxia ◽  
Hypoxia Ischemia

Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), which results in infant cerebral palsy due to the effects on myelination. The origin of OPC vulnerability in HIBD, however, remains controversial. In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity (DEHSI) in postnatal 7-day-old rats. The electrophysiological functional properties of OPCs in HIBD were recorded by patch-clamp in acute cerebral cortex slices. The slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibody to identify local OPCs. Passive membrane properties and K+ channel functions in OPCs were analyzed to estimate the onset of vulnerability in HIBD. The resting membrane potential, membrane resistance, and membrane capacitance of OPCs were increased in both the gray and white matter of the cerebral cortex. OPCs in both the gray and white matter exhibited voltage-dependent K+ currents, which consisted of the initiated rectified potassium currents ( IA) and the sustained rectified currents ( IK). The significant alternation in membrane resistance was influenced by the diversity of potassium channel kinetics. These findings suggest that the rectification of IA and IK channels may play a significant role in OPC vulnerability in HIBD.

Expression of ephrinB2 and EphB4 in a neonatal rat model of periventricular white matter damage

2015 ◽  
Vol 43 (3) ◽  
Author(s):  
Lihua Zhu ◽  
Lijuan Qian ◽  
Shiyu Wang ◽  
Ting Wang ◽  
Li Jiang
Keyword(s):  
White Matter ◽  
Rat Model ◽  
Vascular System ◽  
Periventricular Leukomalacia ◽  
Vascular Supply ◽  
Neonatal Rat ◽  
Cerebral White Matter ◽  
Periventricular White Matter ◽  
White Matter Damage ◽  
Hypoxia Ischemia

AbstractPeriventricular white matter damage (PWMD), also termed periventricular leukomalacia, is the predominant neurologic lesion in preterm infants. It appears to relate in part to the development of the vascular supply to the cerebral white matter. We investigated whether, in case of severe hypoxia-ischemia, the vascular system would be subject to severe damage or remodeled.To evaluate microvessel density (MVD) and the use of ephrinB2 and its receptor EphB4 to mark arterioles and venules to establish the correct anatomic assignment of the remodeled vessels in a hypoxia-induced PWMD rat model.Postnatal day 3 rats underwent permanent ligation of the right common carotid artery followed by 6% OCompared with sham rats, MVD, ephrinB2 and EphB4 levels were higher in the brains of hypoxic-ischemic rats. Similar percentages of vessels expressed ephrinB2 and EphB4 in sham rats, but expression of ephrinB2 was greater in brains injured by hypoxia-ischemia.Following hypoxic-ischemic injury to the rat brain, microvessels were remodeled and more arterioles than venules were acquired.

scholarly journals Circular RNA Expression in the Brain of a Neonatal Rat Model of Periventricular White Matter Damage

2018 ◽  
Vol 49 (6) ◽  
pp. 2264-2276 ◽  
Author(s):  
Lihua Zhu ◽  
Ruibin Zhao ◽  
Li Huang ◽  
Sisi Mo ◽  
Zhangbin Yu ◽  
...  
Keyword(s):  
White Matter ◽  
Target Genes ◽  
Expression Profiles ◽  
Pcr Analysis ◽  
Periventricular White Matter ◽  
White Matter Damage ◽  
Qrt Pcr ◽  
Hypoxia Ischemia ◽  
The Brain ◽  
Brain Tissues

Background/Aims: Periventricular white matter damage (PWMD) is the predominant neurologic lesion in preterm infants who survive brain injury. In this study, we assessed the global changes in and characteristics of the transcriptome of circular RNAs (circRNAs) in the brain tissues of rats with PWMD. Methods: We compared the expression profiles of circRNAs in brain samples from three rats with PWMD and three paired control tissues using deep RNA sequencing. Bioinformatics analysis was applied to investigate these differentially expressed circRNAs, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis was performed to confirm the results. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to predict associated cell signaling pathways and functions. Network analysis was performed to predict circRNAs-microRNAs, and target genes related to PWMD. Results: A total of 2151 more reliable circRNAs were dysregulated in the brain tissues of rats with PWMD, indicating a potential role in the condition. Of the 98 circRNAs significantly differentially expressed in rat brains with PWMD (P< 0.05), 52 were significantly over-expressed and 46 were significantly under-expressed. The expression profiles of seven of 10 randomly selected circRNAs were confirmed by qRT-PCR analysis. The glutamatergic synapse pathway and the VEGF signaling pathway, both associated with hypoxia/ischemia induced brain damage, were inriched. Relationship between miRNA (rno-miR-433-3p and rno-miR-206-3p) and HIF-1α were evident and potential associations between chr6: 48820833|48857932 and their target genes (rno-miR-433-3p and rno-miR-206-3p) were identified. Conclusion: The distinct expression patterns of circRNAs in the brain tissues of rats with PWMD suggest that circRNAs actively respond to hypoxia-ischemia. These findings could assist the development of novel diagnostic and therapeutic targets for PWMD therapy.

scholarly journals Timing of Appearance of Late Oligodendrocyte Progenitors Coincides with Enhanced Susceptibility of Preterm Rabbit Cerebral White Matter to Hypoxia-Ischemia

2010 ◽  
Vol 30 (5) ◽  
pp. 1053-1065 ◽  
Author(s):  
Joshua R Buser ◽  
Kristen N Segovia ◽  
Justin M Dean ◽  
Kerst Nelson ◽  
Douglas Beardsley ◽  
...  
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
Rabbit Model ◽  
White Matter Lesions ◽  
White Matter Injury ◽  
Microvascular Blood Flow ◽  
Cerebral White Matter ◽  
Caspase Activation ◽  
Oligodendrocyte Progenitors ◽  
Hypoxia Ischemia

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.

scholarly journals Identification of Bax-Interacting Proteins in Oligodendrocyte Progenitors during Glutamate Excitotoxicity and Perinatal Hypoxia–Ischemia

ASN NEURO ◽  
2013 ◽  
Vol 5 (5) ◽  
pp. AN20130027 ◽  
Author(s):  
Sopio Simonishvili ◽  
Mohit Raja Jain ◽  
Hong Li ◽  
Steven W. Levison ◽  
Teresa L. Wood
Keyword(s):  
Glutamate Excitotoxicity ◽  
Interacting Proteins ◽  
Perinatal Hypoxia ◽  
Oligodendrocyte Progenitors ◽  
Hypoxia Ischemia

Oxygen treatment after perinatal hypoxia-ischemia reduces neuronal damage at short survival times, but worsens injury with long-term survival

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S444-S444 ◽  
Author(s):  
Kristin M Noppens ◽  
J Regino Perez-Polo ◽  
David K Rassin ◽  
Karin N Westlund ◽  
Roderic Fabian ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Perinatal Hypoxia ◽  
Survival Times ◽  
Term Survival ◽  
Long Term Survival ◽  
Short Survival ◽  
Oxygen Treatment ◽  
Hypoxia Ischemia
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