White Matter Injury in the Preterm Neonate: The Role of Perfusion

2001 ◽  
Vol 23 (3) ◽  
pp. 209-212 ◽  
Author(s):  
Gorm Greisen ◽  
Klaus Børch
Keyword(s):  
White Matter ◽  
Preterm Neonate ◽  
White Matter Injury

scholarly journals Important Role of Reverse Na+-Ca2+Exchange in Spinal Cord White Matter Injury at Physiological Temperature

2000 ◽  
Vol 84 (2) ◽  
pp. 1116-1119 ◽  
Author(s):  
Shuxin Li ◽  
Qiubo Jiang ◽  
Peter K. Stys
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Traumatic Injury ◽  
White Matter Injury ◽  
Mechanical Trauma ◽  
White Matter Tracts ◽  
Physiological Temperature ◽  
Cord Injury ◽  
Cellular Ca

Spinal cord injury is a devastating condition in which most of the clinical disability results from dysfunction of white matter tracts. Excessive cellular Ca2+ accumulation is a common phenomenon after anoxia/ischemia or mechanical trauma to white matter, leading to irreversible injury because of overactivation of multiple Ca2+-dependent biochemical pathways. In the present study, we examined the role of Na+-Ca2+ exchange, a ubiquitous Ca2+ transport mechanism, in anoxic and traumatic injury to rat spinal dorsal columns in vitro. Excised tissue was maintained in a recording chamber at 37°C and injured by exposure to an anoxic atmosphere for 60 min or locally compressed with a force of 2 g for 15 s. Mean compound action potential amplitude recovered to ≈25% of control after anoxia and to ≈30% after trauma. Inhibitors of Na+-Ca2+ exchange (50 μM bepridil or 10 μM KB-R7943) improved functional recovery to ≈60% after anoxia and ≈70% after traumatic compression. These inhibitors also prevented the increase in calpain-mediated spectrin breakdown products induced by anoxia. We conclude that, at physiological temperature, reverse Na+-Ca2+exchange plays an important role in cellular Ca2+ overload and irreversible damage after anoxic and traumatic injury to dorsal column white matter tracts.

scholarly journals A Systematic Review of WNT Signaling in Endothelial Cell Oligodendrocyte Interactions: Potential Relevance to Cerebral Small Vessel Disease

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1545
Author(s):  
Narek Manukjan ◽  
Zubair Ahmed ◽  
Daniel Fulton ◽  
W. Matthijs Blankesteijn ◽  
Sébastien Foulquier
Keyword(s):  
White Matter ◽  
Small Vessel Disease ◽  
Clinical Manifestations ◽  
Cell Types ◽  
Cerebral Small Vessel Disease ◽  
White Matter Injury ◽  
Small Vessel ◽  
Limited Attention ◽  
Vessel Disease

Key pathological features of cerebral small vessel disease (cSVD) include impairment of the blood brain barrier (BBB) and the progression of white matter lesions (WMLs) amongst other structural lesions, leading to the clinical manifestations of cSVD. The function of endothelial cells (ECs) is of major importance to maintain a proper BBB. ECs interact with several cell types to provide structural and functional support to the brain. Oligodendrocytes (OLs) myelinate axons in the central nervous system and are crucial in sustaining the integrity of white matter. The interplay between ECs and OLs and their precursor cells (OPCs) has received limited attention yet seems of relevance for the study of BBB dysfunction and white matter injury in cSVD. Emerging evidence shows a crosstalk between ECs and OPCs/OLs, mediated by signaling through the Wingless and Int-1 (WNT)/β-catenin pathway. As the latter is involved in EC function (e.g., angiogenesis) and oligodendrogenesis, we reviewed the role of WNT/β-catenin signaling for both cell types and performed a systematic search to identify studies describing a WNT-mediated interplay between ECs and OPCs/OLs. Dysregulation of this interaction may limit remyelination of WMLs and render the BBB leaky, thereby initiating a vicious neuroinflammatory cycle. A better understanding of the role of this signaling pathway in EC–OL crosstalk is essential in understanding cSVD development.

scholarly journals 6-Gingerol Alleviates Neonatal Hypoxic-Ischemic Cerebral and White Matter Injury and Contributes to Functional Recovery

2021 ◽  
Vol 12 ◽  
Author(s):  
Man Zhao ◽  
Yuan Yao ◽  
Jingyi Du ◽  
Liang Kong ◽  
Tiantian Zhao ◽  
...  
Keyword(s):  
Cell Death ◽  
White Matter ◽  
Inflammatory Responses ◽  
Epigenetic Modification ◽  
Pathological Process ◽  
White Matter Injury ◽  
Inflammatory Factor ◽  
Ginger Extract ◽  
Motor Disability

Hypoxic-ischemic encephalopathy (HIE) is one main cause of neonatal death and disability, causing substantial injury to white and gray matter, which can lead to severe neurobehavioral dysfunction, including intellectual disability and dyskinesia. Inflammation, nerve cell death, and white matter injury are important factors in the pathological process of HIE. 6-Gingerol is a ginger extract, which reduces inflammatory response and cell death. However, the role of 6-Gingerol in neonatal hypoxic-ischemic brain injury (HIBI) remains unknown. In this study, we constructed a mouse HIBI model and analyzed the protective effect of 6-Gingerol on HIBI by using behavioral tests, histological staining, qPCR and western blot. Here, we found that 6-Gingerol treatment could alleviate HIBI and improve short-term reflex performance, which is closely related to cell death and neuroinflammation. Additionally, 6-Gingerol reduced neuronal apoptosis, pro-inflammatory factor release, as well as microglial activation. Furthermore, 6-Gingerol significantly improved motor disability, which is associated with white matter damage. Thus, our results showed that 6-Gingerol could reduce the loss of myelin sheaths, alleviate cell death of oligodendrocytes, and stimulate the maturation of oligodendrocytes. In terms of mechanism, we found that 6-Gingerol decreased histone H3K27me3 levels, activated AKT pathway and inhibited the activation of ERK and NF-κB pathway at 3 days post-HIBI. Taken together, our data clearly indicate that 6-Gingerol plays a neuroprotective role against HIBI by epigenetic modification and regulation of AKT, ERK, and NF-κB pathways, inhibiting inflammatory responses and reducing cell death.

scholarly journals The immune-inflammatory response of oligodendrocytes in a murine model of preterm white matter injury: the role of TLR3 activation

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Marta Boccazzi ◽  
Juliette Van Steenwinckel ◽  
Anne-Laure Schang ◽  
Valérie Faivre ◽  
Tifenn Le Charpentier ◽  
...  
Keyword(s):  
White Matter ◽  
Primary Cultures ◽  
White Matter Injury ◽  
Poly I:C ◽  
Cytokines And Chemokines ◽  
Wide Range ◽  
Preterm Born ◽  
And Function

AbstractA leading cause of preterm birth is the exposure to systemic inflammation (maternal/fetal infection), which leads to neuroinflammation and white matter injury (WMI). A wide range of cytokines and chemokines are expressed and upregulated in oligodendrocytes (OLs) in response to inflammation and numerous reports show that OLs express several receptors for immune related molecules, which enable them to sense inflammation and to react. However, the role of OL immune response in WMI is unclear. Here, we focus our study on toll-like receptor-3 (TLR3) that is activated by double-strand RNA (dsRNA) and promotes neuroinflammation. Despite its importance, its expression and role in OLs remain unclear. We used an in vivo mouse model, which mimics inflammation-mediated WMI of preterm born infants consisting of intraperitoneal injection of IL-1β from P1 to P5. In the IL-1β-treated animals, we observed the upregulation of Tlr3, IL-1β, IFN-β, Ccl2, and Cxcl10 in both PDGFRα+ and O4+ sorted cells. This upregulation was higher in O4+ immature OLs (immOLs) as compared to PDGFRα+ OL precursor cells (OPCs), suggesting a different sensitivity to neuroinflammation. These observations were confirmed in OL primary cultures: cells treated with TLR3 agonist Poly(I:C) during differentiation showed a stronger upregulation of Ccl2 and Cxcl10 compared to cells treated during proliferation and led to decreased expression of myelin genes. Finally, OLs were able to modulate microglia phenotype and function depending on their maturation state as assessed by qPCR using validated markers for immunomodulatory, proinflammatory, and anti-inflammatory phenotypes and by phagocytosis and morphological analysis. These results show that during inflammation the response of OLs can play an autonomous role in blocking their own differentiation: in addition, the immune activation of OLs may play an important role in shaping the response of microglia during inflammation.

White matter injury in the immature brain: role of interleukin-18

2004 ◽  
Vol 373 (1) ◽  
pp. 16-20 ◽  
Author(s):  
Maj Hedtjärn ◽  
Carina Mallard ◽  
Pernilla Arvidsson ◽  
Henrik Hagberg
Keyword(s):  
White Matter ◽  
White Matter Injury ◽  
Interleukin 18 ◽  
Immature Brain

Mr Imaging of Spastic Diplegia

1996 ◽  
Vol 37 (3P2) ◽  
pp. 830-836 ◽  
Author(s):  
K. Hayakawa ◽  
T. Kanda ◽  
K. Hashimoto ◽  
Y. Okuno ◽  
Y. Yamori ◽  
...  
Keyword(s):  
White Matter ◽  
Corpus Callosum ◽  
Mr Imaging ◽  
White Matter Injury ◽  
Cerebral White Matter ◽  
Spastic Diplegia ◽  
Preterm Children ◽  
Normal Controls ◽  
Sensitive Marker

Purpose: The MR findings in patients with spastic diplegia were investigated and the role of MR imaging in assessing the extent of brain injury was evaluated. Material and Methods: 39 male and 24 female patients (preterm/term 43/20) were imaged using a 0.5 T MR system. Results: The MR findings in term patients were quite different from those in preterm patients; 55% of the term patients showed normal and minimal changes on MR, whereas 90.7% of the 43 preterm children had periventricular leucomalacia. The deep cerebral white matter was the most frequently involved site. Objective measurements revealed significant reductions of the entire sagittal area of corpus callosum in diplegic patients in comparison with normal controls. The motor palsy severity correlated well with the extent of corpus callosum involvement. Conclusion: The corpus callosum appears to be a sensitive marker site for the assessment of the extent of white matter injury.

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