An Integrated Stroke Model with a Consistent Penumbra for the Assessment of Neuroprotective Interventions

Yang, Dong; Nakajo, Yukako; Iihara, Koji; Kataoka, Hiroharu; Nakagawara, Jyoji; Zhao, Qiang; Yanamoto, Hiroji

doi:10.1159/000356048

Cited by 11 publications

(17 citation statements)

References 140 publications

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“…The method does not use any foreign materials to occlude the lumen of the vessels and consistently produces focal ischemia, regional cerebral blood flow that is .10% but ,20%, and adequate reperfusion in the cortex, achieving good reproducibility for the homogeneous development of cortical infarction. 39 When this method was used to evaluate the susceptibility of PS-K196E mice and PS-KO mice to cerebral ischemia-reperfusion injury, we found that these PS-modified mice did not show any increase in brain infarct volume compared with wild-type control mice. PS protects neurons from ischemic injury in mouse stroke models.…”

Section: Discussionmentioning

confidence: 87%

“…Because of some limitations of the nylon-thread-induced ischemia/reperfusion MCA occlusion brain injury methodology, 46 we employed the 3-VO technique for rodent ischemic stroke. 38,39 This method consists of temporary occlusion of both common carotid arteries in conjunction with permanent unilateral occlusion of an MCA. The method does not use any foreign materials to occlude the lumen of the vessels and consistently produces focal ischemia, regional cerebral blood flow that is .10% but ,20%, and adequate reperfusion in the cortex, achieving good reproducibility for the homogeneous development of cortical infarction.…”

Section: Discussionmentioning

confidence: 99%

“…38,39 In brief, the left common carotid artery was isolated and occluded by a vascular clip (1-vessel occlusion [1-VO]) under halothane inhalation-anesthesia. A skin incision was made at the midpoint between the left orbit and the external auditory canal.…”

Section: Transient Middle Cerebral Artery (Mca) Occlusion Modelmentioning

confidence: 99%

“…During the operation, blood pressure was monitored by an indirect blood pressure meter (BP-98A; Softron, Tokyo, Japan) and rectal temperature was regulated within the range of 36.5 to 37.5°C by a temperature controller (NS-TC10; Neuroscience, Tokyo, Japan). After 24 hours, neurologic deficits were assessed using a scoring scale (from 0 to 4) as described previously, 38,39 and the brains were excised and stained with 2,3,5-triphenyl tetrazolium chloride. The infarcted and the total hemispheric areas of each section were measured using a computer-assisted image-analysis system (WinROOF; Mitani, Tokyo, Japan).…”

Section: Transient Middle Cerebral Artery (Mca) Occlusion Modelmentioning

confidence: 99%

“…The infarcted and the total hemispheric areas of each section were measured using a computer-assisted image-analysis system (WinROOF; Mitani, Tokyo, Japan). 31,39 The infarct volume was adjusted for edema by dividing the volume by the edema index (left hemisphere volume/right hemisphere volume).…”

Section: Transient Middle Cerebral Artery (Mca) Occlusion Modelmentioning

confidence: 99%

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Exacerbated venous thromboembolism in mice carrying a protein S K196E mutation

Banno

Kita

Fernández

et al. 2015

Blood

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Key Points• A protein S-K196E mutation reduced its activated protein C cofactor activity in recombinant murine protein S-K196E and in K196E mutant mice.• Mice carrying a protein S-K196E mutation or heterozygous protein S deficiency were more vulnerable to venous thrombosis than wild-type mice.Protein S (PS) acts as an anticoagulant cofactor for activated protein C in regulation of blood coagulation. The K196E mutation in PS is a race-specific genetic risk factor for venous thromboembolism with a prevalence of ∼2% within the Japanese population. To evaluate the thrombosis risk of the PS-K196E mutation, we generated PS-K196E knockin mice and heterozygous PS-deficient mice. We analyzed their thrombotic states, comparing with mice carrying the factor V Leiden mutation (FV-R504Q), a race-specific genetic risk for venous thrombosis in whites. PS-K196E mice grew normally but had decreased activated protein C cofactor activity in plasma. Purified recombinant murine PS-K196E showed the same decreased activated protein C cofactor activity. A deep vein thrombosis model of electrolytic inferior vena cava injury and pulmonary embolism models induced by infusion of tissue factor or polyphosphates revealed that PS-K196E mice, heterozygous PS-deficient mice, and FV-R504Q mice were much more susceptible to venous thrombosis compared with wild-type mice. Transient middle cerebral artery ischemiareperfusion injury model studies demonstrated that both PS-K196E mice and heterozygous PS-deficient mice had cerebral infarction similar to wild-type mice, consistent with human observations. Our in vitro and in vivo results support a causal relationship between the PS-K196E mutation and venous thrombosis and indicate that PS-K196E mice can provide an in vivo evaluation system to help uncovering racial differences in thrombotic

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Transient Middle Cerebral Artery (Mca) Occlusion Modelmentioning

confidence: 99%

Section: Transient Middle Cerebral Artery (Mca) Occlusion Modelmentioning

confidence: 99%

Section: Transient Middle Cerebral Artery (Mca) Occlusion Modelmentioning

confidence: 99%

See 3 more Smart Citations

Exacerbated venous thromboembolism in mice carrying a protein S K196E mutation

Banno

Kita

Fernández

et al. 2015

Blood

Self Cite

View full text Add to dashboard Cite

show abstract

Animal models of stroke

Zhang

2021

Anim Models and Exp Med

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Stroke is a leading cause of morbidity and mortality worldwide and in China. In China, stroke was the leading cause of death and DALYs in 2017. 1 Age-standardized DALYs per 100 000 population decreased by 33.1% for stroke. Of all strokes, up to 80% to 85% are ischemic, 2 which can be subdivided based on the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification. 3 Large vessel atherosclerosis of cervical or proximal intracranial vessels comprises a major cause of acute stroke, ranging from 30% to 43%, while 20%-31% is caused by cardioembolism. Approximately 10%-23% of all strokes are lacunar in type, which are mainly caused by diabetes and hypertension. Some additional unusual causes, such as vasculopathy or extracranial artery dissection, account for 2%-11%. 4,5 Approximately 5%-21% of strokes are hemorrhagic, and their common causes are hypertension and vascular malformations. 6 Strokes are heterogeneous diseases, and in vivo models are essential tools to mimic these processes for investigating pathophysiology and therapeutic approaches. Each model has its unique strengths and weaknesses (Tables 1 and 2). Only when we realize their importance can we choose the best one for an investigation, with "best" referring to that which most closely approximates a certain aspect of the multiple facets of strokes.

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In Vitro Models of Brain Disorders

Feber

2019

Advances in Neurobiology

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An Integrated Stroke Model with a Consistent Penumbra for the Assessment of Neuroprotective Interventions

Cited by 11 publications

References 140 publications

Exacerbated venous thromboembolism in mice carrying a protein S K196E mutation

Exacerbated venous thromboembolism in mice carrying a protein S K196E mutation

Animal models of stroke

In Vitro Models of Brain Disorders

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