The axon–glia unit in white matter stroke: Mechanisms of damage and recovery

Rosenzweig, Shira; Carmichael, S. Thomas

doi:10.1016/j.brainres.2015.02.019

Cited by 55 publications

(44 citation statements)

References 169 publications

(178 reference statements)

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“…Remyelination is critical for recovery in several diseases, such as MS, neonatal white matter injury (NWMI) and stroke (Franklin and Ffrench-Constant, 2008; Rosenzweig and Carmichael, 2015). In these conditions, OPCs often fail to differentiate into mature OLs required for myelin repair (Fancy et al, 2011a).…”

Section: Introductionmentioning

confidence: 99%

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage

Petersen

Ryu

Chang

et al. 2017

Neuron

150

153

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Summary Blood-brain barrier (BBB) disruption alters the composition of the brain microenvironment by allowing blood proteins into the CNS. However, whether blood-derived molecules serve as extrinsic inhibitors of remyelination is unknown. Here we show that the coagulation factor fibrinogen activates the bone morphogenetic protein (BMP) signaling pathway in oligodendrocyte progenitor cells (OPCs) and suppresses remyelination. Fibrinogen induces phosphorylation of Smad 1/5/8 and inhibits OPC differentiation into myelinating oligodendrocytes (OLs), while promoting an astrocytic fate in vitro. Fibrinogen effects are rescued by BMP type I receptor inhibition using dorsomorphin homologue 1 (DMH1) or CRISPR/Cas9 activin A receptor type I (ACVR1) knockout in OPCs. Fibrinogen and the BMP target Id2 are increased in demyelinated multiple sclerosis (MS) lesions. Therapeutic depletion of fibrinogen decreases BMP signaling and enhances remyelination in vivo. Targeting fibrinogen may be an upstream therapeutic strategy to promote the regenerative potential of CNS progenitors in diseases with remyelination failure.

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Section: Introductionmentioning

confidence: 99%

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage

Petersen

Ryu

Chang

et al. 2017

Neuron

150

153

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“…The WM microstructure is determined by its composition. Previous reviews have summarized the microstructure of the white matter in detail, such as the review by Wang Yuan and Rosenzweig Shira . In addition, myelinated axons have a unique molecular structure and organization that enable them to quickly and efficiently transmit the action potentials .…”

Section: The Organization and Function Of White Mattermentioning

confidence: 99%

“…Previous reviews have summarized the microstructure of the white matter in detail, such as the review by Wang Yuan 19 and Rosenzweig Shira. 20 In addition, myelinated axons have a unique molecular structure and organization that enable them to quickly and efficiently transmit the action potentials. 21 Glial cells in the white matter of the brain have been reported to be implicated in the WMI.…”

Section: The Org Aniz Ati On and Fun C Ti On Of White Mat Termentioning

confidence: 99%

“…Many studies have explored the pathophysiology of WMI after cerebral hemorrhage, including direct compression and barotrauma caused by hematoma, hemodynamic changes caused by ischemia, cerebral edema, destruction of the blood-brain barrier, effects of red blood cell breakdown products, excitatory toxic effects, oxidative stress, neuroinflammation, and apoptosis. 19,20,26,27 Many mechanisms about WMI after ICH have been summarized by these above reviews, and recent findings suggest that some molecular signaling pathways involve the process. The elevation of prostaglandin level after cerebral hemorrhage, particularly PEG1, PEG2, and PEG3, can be mediated by interaction with four different G protein-coupled receptors expressed by neurons and glial cells.…”

Section: Pathophys I Ology Of Wmi Af Ter Ichmentioning

confidence: 99%

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White matter repair and treatment strategy after intracerebral hemorrhage

et al. 2019

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The predilection site of intracerebral hemorrhage (ICH) is in the basal ganglia, which is rich in white matter (WM) fiber bundles, such as cerebrospinal tract in the internal capsule. ICH induced damage to this area can easily lead to severe neurological dysfunction and affects the prognosis and quality of life of patients. At present, the pathophysiological mechanisms of white matter injury (WMI) after ICH have attracted researchers' attention, but studies on the repair and recovery mechanisms and therapy strategies remain rare. In this review, we mainly summarized the WM recovery and treatment strategies after ICH by updating the WMI‐related content by reviewing the latest researches and proposing the bottleneck of the current research.

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“…Classic examples for such pathological conditions are the major human demyelinating disease, Multiple Sclerosis (MS), and the dysmyelinating genetic disorders grouped under the term leukodystrophies (Griffin and Lassman, 2004). More recently, myelin dysfunction and/or damage has also been associated with ischemic and traumatic brain injury (Armstrong et al, 2015; Back and Rosenberg, 2014; Rosenzweig and Carmichael, 2015), perinatal white matter injury/periventricular leukomalacia (Back, 2015; Folkerth, 2006; Haynes et al, 2003; Volpe, 2009), as well as neuropsychiatric diseases (Haroutunian et al, 2014; Miguel-Hidalgo, 2013; Nave and Ehrenreich, 2014). In light of the disabling burden of all of the above mentioned neurologic disorders, there is the hope that our progressive biological understanding of the OLG and the regulation of CNS myelination will lead to therapeutic approaches aimed at the regeneration of the myelin sheath as a critical step toward curative treatments.…”

Section: Introductionmentioning

confidence: 99%

Extracellular cues influencing oligodendrocyte differentiation and (re)myelination

Wheeler

Fuss

2016

Experimental Neurology

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There is an increasing number of neurologic disorders found to be associated with loss and/or dysfunction of the CNS myelin sheath, ranging from the classic demyelinating disease, Multiple Sclerosis, through CNS injury, to neuropsychiatric diseases. The disabling burden of these diseases has sparked a growing interest in gaining a better understanding of the molecular mechanisms regulating the differentiation of the myelinating cells of the CNS, oligodendrocytes (OLGs), and the process of (re)myelination. In this context, the importance of the extracellular milieu is becoming increasingly recognized. Under pathological conditions, changes in inhibitory as well as permissive/promotional cues are thought to lead to an overall extracellular environment that is obstructive for the regeneration of the myelin sheath. Given the general view that remyelination is, even though limited in human, a natural response to demyelination, targeting pathologically ‘dysregulated’ extracellular cues and their downstream pathways is regarded as a promising approach toward the enhancement of remyelination by endogenous (or if necessary transplanted) OLG progenitor cells. In this review, we will introduce the extracellular cues that have been implicated in the modulation of (re)myelination. These cues can be soluble, part of the extracellular matrix (ECM) or mediators of cell-cell interactions. Their inhibitory and permissive/promotional roles with regard to remyelination as well as their potential for therapeutic intervention will be discussed.

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The axon–glia unit in white matter stroke: Mechanisms of damage and recovery

Cited by 55 publications

References 169 publications

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage

White matter repair and treatment strategy after intracerebral hemorrhage

Extracellular cues influencing oligodendrocyte differentiation and (re)myelination

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