Marked, sustained expression of a novel 150-kDa oxygen-regulated stress protein, in severely ischemic mouse neurons

Matsushita, Kohji; Matsuyama, Tomohiro; Nishimura, Hiroyuki; Takaoka, Toshio; Kuwabara, Kosuke; Tsukamoto, Yoshitane; Sugita, Minoru; Ogawa, Satoshi

doi:10.1016/s0169-328x(98)00174-0

Cited by 42 publications

(25 citation statements)

References 39 publications

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“…Cerebral blood flow in the MCA area was monitored as described. 19 All mice showed a Ͼ75% decrease in cerebral blood flow rapidly after occlusion and restored cerebral blood flow (Ͼ0%) soon after reperfusion compared with before transient ligation of the MCA. tPA (10 mg/kg body weight in 0.1 mL saline; Mitsubishi Tanabe Pharmaceutical Co, Tokyo, Japan) was infused through the tail vein just before reperfusion.…”

Section: Induction Of Focal Cerebral Ischemiamentioning

confidence: 92%

Cilostazol Reduces the Risk of Hemorrhagic Infarction After Administration of Tissue-Type Plasminogen Activator in a Murine Stroke Model

Kasahara

Nakagomi

Matsuyama

et al. 2012

Stroke

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Background and Purpose-Prior use of antiplatelet agents improves stroke outcome in patients undergoing thrombolytic therapy as shown by reduced arterial reocclusion, although the risk of cerebral hemorrhage can be increased. Methods-The effect of cilostazol, an antiplatelet drug that improves endothelial function through upregulation of intracellular cAMP, on cerebral hemorrhage after thrombolytic therapy was investigated using a highly reproducible transient ischemia model. Results-Treatment with cilostazol for 7 days before ischemia significantly suppressed the risk and severity of cerebral hemorrhage after injection of tissue-type plasminogen activator, although treatment with aspirin had no such protective effect compared with nontreated mice. Immunohistological analysis revealed that treatment with cilostazol suppressed disruption of the microvasculature in the ischemic area associated with reduced matrix metalloproteinase-9 activity. Conclusions-Our results suggest that patients treated with cilostazol before onset of stroke could have a lower risk of cerebral hemorrhage after thrombolytic therapy and might also have a longer therapeutic time window for thrombolysis. Furthermore, the risk of cerebral hemorrhage can be significantly altered by prestroke therapies, and analysis of the effects of multiple drugs on tissue-type plasminogen activator-induced cerebral hemorrhage in animal models is essential for the extending safe and effective thrombolytic therapy to a wider group of patients.

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Section: Induction Of Focal Cerebral Ischemiamentioning

confidence: 92%

Cilostazol Reduces the Risk of Hemorrhagic Infarction After Administration of Tissue-Type Plasminogen Activator in a Murine Stroke Model

Kasahara

Nakagomi

Matsuyama

et al. 2012

Stroke

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“…Under halothane inhalation (3%), the left MCA was isolated, electrocauterized, and disconnected just distal to its crossing of the olfactory tract (distal M1 portion). CBF in the MCA area was monitored as described (41). Mice that showed decreased CBF by approximately 75% immediately after and 24 hours after ligation were used for our experiments (success rate of >95%).…”

Section: Methodsmentioning

confidence: 99%

Administration of CD34+ cells after stroke enhances neurogenesis via angiogenesisin a mouse model

Taguchi¹,

Soma²,

Tanaka³

et al. 2004

J. Clin. Invest.

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658

433

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Thrombo-occlusive cerebrovascular disease resulting in stroke and permanent neuronal loss is an important cause of morbidity and mortality. Because of the unique properties of cerebral vasculature and the limited reparative capability of neuronal tissue, it has been difficult to devise effective neuroprotective therapies in cerebral ischemia. Our results demonstrate that systemic administration of human cord blood-derived CD34 + cells to immunocompromised mice subjected to stroke 48 hours earlier induces neovascularization in the ischemic zone and provides a favorable environment for neuronal regeneration. Endogenous neurogenesis, suppressed by an antiangiogenic agent, is accelerated as a result of enhanced migration of neuronal progenitor cells to the damaged area, followed by their maturation and functional recovery. Our data suggest an essential role for CD34 + cells in promoting directly or indirectly an environment conducive to neovascularization of ischemic brain so that neuronal regeneration can proceed.

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“…This is part of the ER machinery that imports proteins from the secretory pathway into the ER, and together with other chaperones such as 78-and 94-kDa glucose regulated proteins (GRP 78 and GRP 94) ORP 150 assists in the folding and assembly of secretory and membrane proteins [13]. The expression of ORP 150 becomes increased in a range of pathologic situations such as brain ischaemia [14], atherosclerotic plaques [15] and malignant tumours [16]. The expression of ORP 150 in cultured human cells is essential for their survival under prolonged hypoxia [5].…”

Section: Introductionmentioning

confidence: 99%

The Effect of Hypoxia on the Expression of 150 kDa Oxygen-regulated Protein (ORP 150) in HeLa Cells

Cechowska-Pasko

Bańkowski²,

Chêne³

2006

Cell Physiol Biochem

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Correct protein folding is an important factor, for the translocation of newly synthesised proteins to specific subcellular compartments, extracellular matrix or to biological fluids. This process is regulated by a group of specific proteins, referred to as chaperones. Many stress conditions, such as oxygen or glucose deprivation, slow down the folding process and cause accumulation of unfolded/misfolded proteins in the cell. Molecular chaperones are induced in these conditions; with some named as oxygen-regulated proteins (ORPs). These bind to unfolded / misfolded proteins to facilitate correct assembly. ORP 150 is the subject of this study. Hypoxia results in an enhancement of ORP 150 expression in several tumour cell lines cultured in vitro. HeLa cells grown in hypoxic conditions (despite an intensive expression of ORP 150) demonstrate higher rates of apoptosis in comparison to those cultured in normoxic conditions. Furthermore, the inhibition of ORP 150 synthesis by transfection of these cells with a specific siRNA resulted in an intensification of apoptosis, as indicated by specific markers of this process; the enhancement of poly ADP-ribose protein cleavage and the increase in Bim protein expression. We conclude from our study that the increase in ORP 150 synthesis protects the cells against the proapoptotic effect of hypoxia.

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Marked, sustained expression of a novel 150-kDa oxygen-regulated stress protein, in severely ischemic mouse neurons

Cited by 42 publications

References 39 publications

Cilostazol Reduces the Risk of Hemorrhagic Infarction After Administration of Tissue-Type Plasminogen Activator in a Murine Stroke Model

Cilostazol Reduces the Risk of Hemorrhagic Infarction After Administration of Tissue-Type Plasminogen Activator in a Murine Stroke Model

Administration of CD34+ cells after stroke enhances neurogenesis via angiogenesisin a mouse model

The Effect of Hypoxia on the Expression of 150 kDa Oxygen-regulated Protein (ORP 150) in HeLa Cells

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