scholarly journals White Matter Injury and Recovery after Hypertensive Intracerebral Hemorrhage

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Shilun Zuo ◽  
Pengyu Pan ◽  
Qiang Li ◽  
Yujie Chen ◽  
Hua Feng
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
White Matter Injury ◽  
Pathophysiological Mechanism ◽  
Research Perspective ◽  
Stroke Research ◽  
The Face ◽  
Injury And Repair ◽  
Hypertensive Intracerebral Hemorrhage ◽  
White Matter Repair

Hypertensive intracerebral hemorrhage (ICH) could very probably trigger white matter injury in patients. Through the continuous study of white matter injury after hypertensive ICH, we achieve a more profound understanding of the pathophysiological mechanism of its occurrence and development. At the same time, we found a series of drugs and treatment methods for the white matter repair. In the current reality, the research paradigm of white matter injury after hypertensive ICH is relatively obsolete or incomplete, and there are still lots of deficiencies in the research. In the face of the profound changes of stroke research perspective, we believe that the combination of the lenticulostriate artery, nerve nuclei of the hypothalamus-thalamus-basal ganglia, and the white matter fibers located within the capsula interna will be beneficial to the research of white matter injury and repair. This paper has classified and analyzed the study of white matter injury and repair after hypertensive ICH and also rethought the shortcomings of the current research. We hope that it could help researchers further explore and study white matter injury and repair after hypertensive ICH.

scholarly journals White Matter Injury After Intracerebral Hemorrhage

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiongjie Fu ◽  
Guoyang Zhou ◽  
Jianfeng Zhuang ◽  
Chaoran Xu ◽  
Hang Zhou ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
White Matter Injury ◽  
Neurological Deficits ◽  
Comprehensive Treatment ◽  
High Morbidity ◽  
Pathophysiological Mechanism ◽  
Strongly Correlated ◽  
Long Term Prognosis ◽  
Brain Insults

Spontaneous intracerebral hemorrhage (ICH) accounts for 15% of all stroke cases. ICH is a devastating form of stroke associated with high morbidity, mortality, and disability. Preclinical studies have explored the mechanisms of neuronal death and gray matter damage after ICH. However, few studies have examined the development of white matter injury (WMI) following ICH. Research on WMI indicates that its pathophysiological presentation involves axonal damage, demyelination, and mature oligodendrocyte loss. However, the detailed relationship and mechanism between WMI and ICH remain unclear. Studies of other acute brain insults have indicated that WMI is strongly correlated with cognitive deficits, neurological deficits, and depression. The degree of WMI determines the short- and long-term prognosis of patients with ICH. This review demonstrates the structure and functions of the white matter in the healthy brain and discusses the pathophysiological mechanism of WMI following ICH. Our review reveals that the development of WMI after ICH is complex; therefore, comprehensive treatment is essential. Understanding the relationship between WMI and other brain cells may reveal therapeutic targets for the treatment of ICH.

scholarly journals White matter repair and treatment strategy after intracerebral hemorrhage

2019 ◽  
Vol 25 (10) ◽  
pp. 1113-1125 ◽  
Author(s):  
Yi‐Bin Jiang ◽  
Kai‐Yan Wei ◽  
Xu‐Yang Zhang ◽  
Hua Feng ◽  
Rong Hu
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Treatment Strategy ◽  
White Matter Repair

scholarly journals The effect of age-related risk factors and comorbidities on white matter injury and repair after ischemic stroke

2019 ◽  
Vol 126 ◽  
pp. 13-22 ◽  
Author(s):  
Mingyue Xu ◽  
Michael M. Wang ◽  
Yanqin Gao ◽  
Richard F. Keep ◽  
Yejie Shi
Keyword(s):  
Risk Factors ◽  
Ischemic Stroke ◽  
White Matter ◽  
White Matter Injury ◽  
Age Related ◽  
Related Risk ◽  
Injury And Repair ◽  
Effect Of Age

scholarly journals HDAC inhibition reduces white matter injury after intracerebral hemorrhage

2020 ◽  
pp. 0271678X2094261
Author(s):  
Heng Yang ◽  
Wei Ni ◽  
Pengju Wei ◽  
Sicheng Li ◽  
Xinjie Gao ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Hdac Inhibitor ◽  
Histone Deacetylases ◽  
Macrophage Polarization ◽  
Conditional Knockout ◽  
White Matter Injury ◽  
Hdac Inhibition

Inhibition of histone deacetylases (HDACs) has been shown to reduce inflammation and white matter damage after various forms of brain injury via modulation of microglia/macrophage polarization. Previously we showed that the HDAC inhibitor scriptaid could attenuate white matter injury (WMI) after ICH. To access whether modulation of microglia/macrophage polarization might underlie this protection, we investigated the modulatory role of HDAC2 in microglia/macrophage polarization in response to WMI induced by intracerebral hemorrhage (ICH) and in primary microglia and oligodendrocyte co-cultures. HDAC2 activity was inhibited via conditional knockout of the Hdac2 gene in microglia or via administration of scriptaid. Conditional knockout of the Hdac2 gene in microglia and HDAC inhibition with scriptaid both improved neurological functional recovery and reduced WMI after ICH. Additionally, HDAC inhibition shifted microglia/macrophage polarization toward the M2 phenotype and reduced proinflammatory cytokine secretion after ICH in vivo. In vitro, a transwell co-culture model of microglia and oligodendrocytes also demonstrated that the HDAC inhibitor protected oligodendrocytes by modulating microglia polarization and mitigating neuroinflammation. Moreover, we found that scriptaid decreased the expression of pJAK2 and pSTAT1 in cultured microglia when stimulated with hemoglobin. Thus, HDAC inhibition ameliorated ICH-mediated neuroinflammation and WMI by modulating microglia/macrophage polarization.

Taurine supplementation reduces neuroinflammation and protects against white matter injury after intracerebral hemorrhage in rats

Amino Acids ◽  
2017 ◽  
Vol 50 (3-4) ◽  
pp. 439-451 ◽  
Author(s):  
Hengli Zhao ◽  
Jie Qu ◽  
Qiang Li ◽  
Mengchu Cui ◽  
Jie Wang ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
White Matter Injury ◽  
Taurine Supplementation

Abstract 52: Changes in Oligodendrocyte Sub-Populations After Neonatal Stroke

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Andra Dingman ◽  
Alexandra Frazier ◽  
Katherine Given ◽  
Benjamin Wassermann ◽  
Wendy B Macklin ◽  
...  
Keyword(s):  
Gene Expression ◽  
White Matter ◽  
Single Cell ◽  
Fluorescent Antibody ◽  
Artery Occlusion ◽  
White Matter Injury ◽  
Data Set ◽  
Neonatal Stroke ◽  
Ipsilateral Striatum ◽  
Injury And Repair

Background: Chronic white matter changes after neonatal stroke have not been well studied. Histologically, we see a robust increase in oligodendrocytes (OLs) in injured striatum 14 days post-middle cerebral artery occlusion (MCAO) in neonatal mice. The contribution of these cells to chronic white matter injury and repair has not been evaluated. Objective: Evaluate changes in striatal OL cell gene expression after neonatal MCAO. Methods: Mice underwent 60 minutes of MCAO at postnatal day 10 using the filament model and sacrificed 14 days later for fluorescent antibody cell sorting and single cell RNA sequencing. Single cell suspensions from Injured (ipsilateral) and uninjured (contralateral) striata were incubated with antibodies to immature and mature OLs. Cells expressing OL markers were collected and captured using 10x Genomics Chromium with V3.1 chemistry and analyzed in Seurat V3.1. Results: We captured a total of 4598 cells, with ~250,000 reads per cell. Our data set was comprised of 2399 oligodendrocytes (915 Contralateral, 1484 Ipsilateral). Feature plots of OL markers demonstrate that the entire lineage is present in our cell population (Fig 1A). Unbiased clustering identified 10 sub-populations of oligodendrocytes (Fig 1B). In ipsilateral striatum there was a significant decrease in the proportion of cells in cluster 8 (p <0.0001, proportions test, Fig 1C), which also express OL progenitor cell (OPC) markers. There was a significant increase in the proportion of cells in clusters 1 and 5. Pathway analysis suggest that both these clusters are comprised of pre-myelinating oligodendrocytes. Conclusions: At 14 days after neonatal stroke in mice scSEQ reveals a depletion of an OPC sub-population and an increase in sub-mature clusters of oligodendrocytes in ipsilateral striatum. Ongoing analysis of differential gene expression will reveal new insights into these cells and potential targets to promote white matter repair after neonatal stroke.

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