Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Kathirvelu, Balachandar; Carmichael, S. Thomas

doi:10.1007/s11011-014-9559-7

Cited by 18 publications

(14 citation statements)

References 97 publications

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“…clot-derived cytotoxic factors, neuroinflammation 11–13 ) injury components followed by a period of repair. The therapeutic time window for modulating brain repair may be longer than for preventing ICH-induced brain injury 14 .…”

Section: Modeling Ich-induced Brain Injury and Repair – Areas For Focusmentioning

confidence: 99%

Basic and Translational Research in Intracerebral Hemorrhage

Selim¹,

Hanley²,

Broderick³

et al. 2018

Stroke

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Section: Modeling Ich-induced Brain Injury and Repair – Areas For Focusmentioning

confidence: 99%

Basic and Translational Research in Intracerebral Hemorrhage

Selim¹,

Hanley²,

Broderick³

et al. 2018

Stroke

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“…Compounds currently under study include such drugs as deferoxamine, minocycline, statins, celecoxib, desmopressin, and conivaptan. These drugs each addresses some aspect of the pathology noted in the mechanisms above [ 32 , 34 , 35 ]. Similar to stroke and thrombectomy in the past, advances in ICH treatment have been stalled by a lack of significant positive data supporting evacuation/removal of the hematoma.…”

Section: Conference Proceedings—october 4–5 2017mentioning

confidence: 99%

Uncovering the Rosetta Stone: Report from the First Annual Conference on Key Elements in Translating Stroke Therapeutics from Pre-Clinical to Clinical

Bix

Fraser

Mack

et al. 2018

Transl. Stroke Res.

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The first annual Stroke Translational Research Advancement Workshop (STRAW), entitled “Uncovering the Rosetta Stone: Key Elements in Translating Stroke Therapeutics from Pre-Clinical to Clinical” was held at the University of Kentucky on October 4–5, 2017. This workshop was organized by the Center for Advanced Translational Stroke Science. The workshop consisted of 2 days of activities. These included three presentations establishing the areas of research in stroke therapeutics, discussing the routes for translation from bench to bedside, and identifying successes and failures in the field. On day 2, grant funding opportunities and goals for the National Institute for Neurological Diseases and Stroke were presented. In addition, the meeting also included break-out sessions designed to connect researchers in areas of stroke, and to foster potential collaborations. Finally, the meeting concluded with an open discussion among attendees led by a panel of experts.

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“…Intracerebral hemorrhage (ICH) accounts for about 15% of all strokes, with 1-month mortality rates of 50% in patients after ICH [1]. Previous studies have demonstrated that the Blood–Brain barrier (BBB) integrity was disrupted in brain damage after ICH, leading to neurological deficits, inflammatory responses, and cerebral edema [2,3]. The BBB consists of endothelial cells (ECs), pericytes, astrocytes, neurons, and the extracellular matrix (ECM) [4].…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteases-Mediated Cleavage on β-Dystroglycan May Play a Key Role in the Blood–Brain Barrier After Intracerebral Hemorrhage in Rats

Zhang

et al. 2019

Med Sci Monit

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BackgroundIt is well documented that the Blood–Brain barrier (BBB) can be damaged by matrix metalloproteases (MMPs) after intracerebral hemorrhage (ICH), but little is known about the mechanism of this effect.Material/MethodsWe established an ICH model in rats by injecting collagenase VII into the striatum. Afterwards, intraperitoneal injection of these rats with 40 mg/kg GM6001 (a MMPs inhibitor). The effects of GM6001 on ICH were investigated by neurological severity score, brain water content, Evans blue staining, hematoxylin-eosin staining, immunohistochemical staining, and Western blot assays.ResultsWe demonstrated that the neurological damage caused by ICH was relieved at 5 and 7 days following administration of GM6001. The impaired BBB induced by ICH was improved in response to GM6001 treatment at around 3 days, as evidenced by alleviated cerebral edema, decreased Evans blue extravasation, and a reduction in inflammatory cellular infiltration. Mechanism analysis revealed that ICH induced the generation of β-dystroglycan cleavage, which could be suppressed by GM6001 treatment. Furthermore, we found that recombinant MMP2 and MMP9 triggered the cleavage of β-dystroglycan in vitro, and this action could be inhibited by GM6001 administration.ConclusionsTaken together, our results suggest that MMPs-mediated cleavage on β-dystroglycan may play an important role in BBB after ICH.

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Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Cited by 18 publications

References 97 publications

Basic and Translational Research in Intracerebral Hemorrhage

Basic and Translational Research in Intracerebral Hemorrhage

Uncovering the Rosetta Stone: Report from the First Annual Conference on Key Elements in Translating Stroke Therapeutics from Pre-Clinical to Clinical

Matrix Metalloproteases-Mediated Cleavage on β-Dystroglycan May Play a Key Role in the Blood–Brain Barrier After Intracerebral Hemorrhage in Rats

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