Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus

Fukumizu, Michio; Takashima, Sachio; Becker, Laurence E.

doi:10.1016/0387-7604(95)00103-4

Cited by 38 publications

(19 citation statements)

References 21 publications

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“…We cannot rule out, however, the possibility that phospho-Erk is increased in response to hydrocephalus. Elevated phospho-Erk has been associated with astrogliosis (Mandell and VandenBerg, 1999), a pathological response of astrocytes to many types of brain injury, including hydrocephalus (Fukumizu et al, 1996). Increased GFAP expression observed in severely hydrocephalic Ro1 mice is indicative of astrogliosis, particularly because GFAP levels are not elevated in Ro1 mice with mild hydrocephalus (data not shown).…”

Section: Discussionmentioning

confidence: 93%

Development of Hydrocephalus in Mice Expressing the G_i-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Sweger¹,

Casper²,

Scearce‐Levie³

et al. 2007

J. Neurosci.

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We developed a transgenic mouse line that expresses the G i -coupled RASSL (receptor activated solely by synthetic ligand) Ro1 in astrocytes to study astrocyte-neuronal communication. Surprisingly, we found that all transgenics expressing Ro1 developed hydrocephalus. We analyzed these mice in an effort to develop a new model of hydrocephalus that will further our understanding of the pathophysiology of the disease. Expression of Ro1 was restricted to astrocytes by crossing the transgenic hGFAP-tTA (tet transactivator behind the human glial fibrillary acidic protein promoter) mouse line with the transgenic tetO-Ro1/tetO-LacZ mouse line. This cross produced double-transgenic mice that expressed Ro1 in astrocytes. All double transgenics developed hydrocephalus by postnatal day 15, whereas single-transgenic littermate controls appeared normal. Hydrocephalic Ro1 mice displayed enlarged ventricles, partial denudation of the ependymal cell layer, altered subcommissural organ morphology, and obliteration of the cerebral aqueduct. Severely hydrocephalic mice also had increased levels of phospho-Erk and GFAP expression. Administration of doxycycline to breeding pairs suppressed Ro1 expression and the onset of hydrocephalus in double-transgenic offspring. Ro1 animals maintained on dox did not develop hydrocephalus; however, if taken off doxycycline at weaning, double-transgenic mice developed enlarged ventricles within 7 weeks, indicating that Ro1 expression also induces hydrocephalus in adults. This study discovered a new model of hydrocephalus in which the rate of pathogenesis can be controlled enabling the study of the pathogenesis of both juvenile and adult onset hydrocephalus.

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Section: Discussionmentioning

confidence: 93%

Development of Hydrocephalus in Mice Expressing the G_i-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Sweger¹,

Casper²,

Scearce‐Levie³

et al. 2007

J. Neurosci.

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“…On the other hand, the reactive gliosis was formed following swelling and proliferation of astrocytes, which released plenty of pro-inflammatory factors; and thus it could accelerate the formation of glial scar and prevented the repair of BBB in the peri-ventricular and hippocampus at the chronic stage [9]. Though decreasing the deposition of chondroitin sulfate proteogly, the intracellular and extracellular components of glial scar formed in the long term of spinal cord injury were jointly inhabited by curcumin administration [6].…”

Section: Discussionmentioning

confidence: 98%

Prolonged hydrocephalus induced by intraventricular hemorrhage in rats is reduced by curcumin therapy

Zhang

et al. 2017

Neuroscience Letters

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“…Thus, Fukumizu et al [37, 38] found marked ependymal damage and loss in human neonatal IVH. Mayfrank et al [39] used a pig IVH model with and without tissue plasminogen activator-induced fibrinolysis and, similar to Pang et al [36] in dog, they found marked IVH-induced ependymal damage at 1 and 7 weeks and that was reduced by fibrinolysis.…”

Section: Choroid Plexus As a Site Of Injurymentioning

confidence: 99%

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Xiang

Routhe

Wilkinson

et al. 2017

Fluids Barriers CNS

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While the impact of hemorrhagic and ischemic strokes on the blood–brain barrier has been extensively studied, the impact of these types of stroke on the choroid plexus, site of the blood-CSF barrier, has received much less attention. The purpose of this review is to examine evidence of choroid plexus injury in clinical and preclinical studies of intraventricular hemorrhage, subarachnoid hemorrhage, intracerebral hemorrhage and ischemic stroke. It then discusses evidence that the choroid plexuses are important in the response to brain injury, with potential roles in limiting damage. The overall aim of the review is to highlight deficiencies in our knowledge on the impact of hemorrhagic and ischemic strokes on the choroid plexus, particularly with reference to intraventricular hemorrhage, and to suggest that a greater understanding of the response of the choroid plexus to stroke may open new avenues for brain protection.

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Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus

Cited by 38 publications

References 21 publications

Development of Hydrocephalus in Mice Expressing the G_i-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Development of Hydrocephalus in Mice Expressing the G_i-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Prolonged hydrocephalus induced by intraventricular hemorrhage in rats is reduced by curcumin therapy

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

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Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus

Cited by 38 publications

References 21 publications

Development of Hydrocephalus in Mice Expressing the Gi-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Development of Hydrocephalus in Mice Expressing the Gi-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Prolonged hydrocephalus induced by intraventricular hemorrhage in rats is reduced by curcumin therapy

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Contact Info

Product

Resources

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Development of Hydrocephalus in Mice Expressing the G_i-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

Development of Hydrocephalus in Mice Expressing the G_i-Coupled GPCR Ro1 RASSL Receptor in Astrocytes