Characterization of Endogenous Neural Progenitor Cells after Experimental Ischemic Stroke

Shen, Chiung‐Chyi; Yang, Yi‐Chin; Chiao, Ming‐Tsang; Cheng, Wen-Yu; Tsuei, Yuang-Seng; Ko, Jiunn‐Liang

doi:10.2174/156720210790820208

Cited by 35 publications

(25 citation statements)

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“…NeuN was not co-labeled with BMP7 (data not shown). Considering previous reports that reactive astrocytes re-express nestin in the ischemic brain (Lin et al 1995;Duggal et al 1997;Shen et al 2010), BMP7 might be mostly localized in reactive astrocytes during astroglial scar formation in this study. Noggin expression was examined in the ischemic striatum at 4 weeks, the time point at which noggin was the most increased after MCAO (Fig.…”

Section: Bmp7 Expression In Reactive Astrocytes and Noggin In Activatsupporting

confidence: 59%

Different Temporal Patterns in the Expressions of Bone Morphogenetic Proteins and Noggin During Astroglial Scar Formation After Ischemic Stroke

et al. 2012

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Bone morphogenetic proteins (BMPs) and their antagonists have roles in scar formation and regeneration after central nervous system injuries. However, temporal changes in their expression during astroglial scar formation in the ischemic brain are unknown. Here, we examined protein levels of BMP2, BMP7, and their antagonist noggin in the ischemic brain up to 4 weeks after experimental stroke in mice. BMP2 and BMP7 levels were increased from 1 to 4 weeks in the ischemic brain, and their expression was associated with astrogliosis. BMP7 expression was more intense and co-localized in reactive astrocytes in the ischemic subcortex at 1 week. Noggin expression began to increase after 2 weeks and was further increased at 4 weeks only in the ischemic subcortex, but the intensity was weak compared to the intensity of BMPs. Noggin was co-localized mainly in activated microglia. These findings show that expression of BMPs and noggin differed over time, in intensity and in types of cell, and suggest that BMPs and noggin have different roles in the processes of glial scar formation and neurorestoration in the ischemic brain.

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Section: Bmp7 Expression In Reactive Astrocytes and Noggin In Activatsupporting

confidence: 59%

Different Temporal Patterns in the Expressions of Bone Morphogenetic Proteins and Noggin During Astroglial Scar Formation After Ischemic Stroke

et al. 2012

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“…23 Briefly, the test measures the strength (in g) to hold onto a steel grip-bar (Dyadic Systems, Osaka, Tokyo, Model DPS-5R: range, 0-5 kgf) with forepaws. Plasma osmolality was quantitatively determined using a Micro-Osmometer (Advanced Instruments) according to the manufacturer's instructions.…”

Section: Neurobehavioral and Plasma Osmolality Testingmentioning

confidence: 99%

Hyperglycemia Exacerbates Intracerebral Hemorrhage via the Downregulation of Aquaporin-4

Chiu

Chen

Shen

et al. 2013

Stroke

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Background and Purpose-Intracerebral hemorrhage (ICH) is associated with high mortality and neurological deficits, and concurrent hyperglycemia usually worsens clinical outcomes. Aquaporin-4 (AQP-4) is important in cerebral water movement. Our aim was to investigate the role of AQP-4 in hyperglycemic ICH. Methods-Hyperglycemia was induced by intraperitoneal injection of streptozotocin (STZ; 60 mg/kg) in adult SpragueDawley male rats. ICH was induced by stereotaxic infusion of collagenase/heparin into the right striatum. One set of rats was repeatedly monitored by MRI at 1, 4, and 7 days after ICH induction so as to acquire information on the formation of hematoma and edema. Another set of rats was killed and brains were examined for differences in the degree of hemorrhage and edema, water content, blood-brain barrier destruction, and AQP-4 expression. Results-Hyperglycemia ICH rats exhibited increased brain water content, more severe blood-brain barrier destruction, and greater vasogenic edema as seen on diffusion-weighted MRI. Significant downregulation of AQP-4 was observed in STZ-treated rats after ICH as compared with non-STZ-treated rats. Apoptosis was greater on day 1 after ICH in STZtreated rats. Conclusions-The expression of AQP-4 in the brain is downregulated in hyperglycemic rats as compared with normoglycemic rats after ICH. This change is accompanied by increased vasogenic brain edema and more severe blood-brain barrier destruction. (Stroke. 2013;44:1682-1689.)

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“…It is expressed in a rat cerebral ischemia model where vimentin expression is present in the perinuclear cytoplasm of astrocyte colloid cells and oligodendrocytes. There is increased expression of vimentin during the proliferative response of astrocyte colloid cells after ischemic injury (Shen et al, 2010;Pimentel et al, 2011;Lively et al, 2011). It has been suggested by researches that the distribution of vimentin positive cells are located in neurons surrounding colloid cells, and this distribution is consistent with regions of neuronal necrosis (Joachim et al, 2011;Wurm et al, 2011).…”

Section: Discussionmentioning

confidence: 72%

Changes in hippocampal ultrastructure and vimentin expression in rhesus monkeys following selective deep hypothermia and blood occlusion

Li¹,

Fu²,

Niu³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Previous studies have shown that selective cerebral profound hypothermia combined with antegrade cerebral perfusion can improve resistance to cerebral hypoxia-ischemia in monkeys. The aim of this study was to observe the effect of selective cerebral profound hypothermia on the ultrastructure and vimentin expression in monkey hippocampi after severe cerebral ischemia. Eight healthy adult rhesus monkeys were randomly divided into two groups: profound hypothermia (N = 5) and normothermia (N = 3). Monkeys in the profound hypothermia group underwent bilateral carotid artery and jugular vein occlusion for 10 minutes at room temperature. Ringer's solution at 4°C was then perfused through the right internal carotid artery and out of the right jugular vein, maintaining the brain temperature below 18°C. Sixty minutes later, cerebral blood flow was restored. The normothermia group underwent all procedures with the exception that the Ringer's solution was 37°C during perfusion. All animals in the profound hypothermia group were successfully resuscitated. No significant abnormalities of hippocampal morphology or ultrastructure were observed. In contrast, no monkeys were alive after perfusion in the normothermia group and they had abnormal hippocampal morphology and ultrastructure to different extents. Vimentin expression in the hippocampus was significantly lower in the profound hypothermia group (47.88% ± 1.66) than the normothermia group (79.51% ± 1.00; P < 0.01). We conclude that selective cerebral profound hypothermia following 10-min occlusion of the bilateral common carotid arteries was able to downregulate vimentin expression in the hippocampus and protect it from severe cerebral ischemia.

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Characterization of Endogenous Neural Progenitor Cells after Experimental Ischemic Stroke

Cited by 35 publications

References 0 publications

Different Temporal Patterns in the Expressions of Bone Morphogenetic Proteins and Noggin During Astroglial Scar Formation After Ischemic Stroke

Different Temporal Patterns in the Expressions of Bone Morphogenetic Proteins and Noggin During Astroglial Scar Formation After Ischemic Stroke

Hyperglycemia Exacerbates Intracerebral Hemorrhage via the Downregulation of Aquaporin-4

Changes in hippocampal ultrastructure and vimentin expression in rhesus monkeys following selective deep hypothermia and blood occlusion

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