Please use this identifier to cite or link to this item:
https://doi.org/10.1007/s12975-018-0621-3
DC Field | Value | |
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dc.title | Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury | |
dc.contributor.author | Chen B. | |
dc.contributor.author | Ng G. | |
dc.contributor.author | Gao Y. | |
dc.contributor.author | Low S.W. | |
dc.contributor.author | Sandanaraj E. | |
dc.contributor.author | Ramasamy B. | |
dc.contributor.author | Sekar S. | |
dc.contributor.author | Bhakoo K. | |
dc.contributor.author | Soong T.W. | |
dc.contributor.author | Nilius B. | |
dc.contributor.author | Tang C. | |
dc.contributor.author | Robins E.G. | |
dc.contributor.author | Goggi J. | |
dc.contributor.author | Liao P. | |
dc.date.accessioned | 2020-09-07T04:59:51Z | |
dc.date.available | 2020-09-07T04:59:51Z | |
dc.date.issued | 2019 | |
dc.identifier.citation | Chen B., Ng G., Gao Y., Low S.W., Sandanaraj E., Ramasamy B., Sekar S., Bhakoo K., Soong T.W., Nilius B., Tang C., Robins E.G., Goggi J., Liao P. (2019). Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury. Translational Stroke Research 10 (1) : 91-103. ScholarBank@NUS Repository. https://doi.org/10.1007/s12975-018-0621-3 | |
dc.identifier.issn | 18684483 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/174510 | |
dc.description.abstract | The transient receptor potential melastatin 4 (TRPM4) channel has been suggested to play a key role in the treatment of ischemic stroke. However, in vivo evaluation of TRPM4 channel, in particular by direct channel suppression, is lacking. In this study, we used multimodal imaging to assess edema formation and quantify the amount of metabolically functional brain salvaged after a rat model of stroke reperfusion. TRPM4 upregulation in endothelium emerges as early as 2 h post-stroke induction. Expression of TRPM4 channel was suppressed directly in vivo by treatment with siRNA; scrambled siRNA was used as a control. T2-weighted MRI suggests that TRPM4 inhibition successfully reduces edema by 30% and concomitantly salvages functionally active brain, measured by 18 F-FDG-PET. These in vivo imaging results correlate well with post-mortem 2,3,5-triphenyltetrazolium chloride (TTC) staining which exhibits a 34.9% reduction in infarct volume after siRNA treatment. Furthermore, in a permanent stroke model, large areas of brain tissue displayed both edema and significant reductions in metabolic activity which was not shown in transient models with or without TRPM4 inhibition, indicating that tissue salvaged by TRPM4 inhibition during stroke reperfusion may survive. Evans Blue extravasation and hemoglobin quantification in the ipsilateral hemisphere were greatly reduced, suggesting that TRPM4 inhibition can improve BBB integrity after ischemic stroke reperfusion. Our results support the use of TRPM4 blocker for early stroke reperfusion. © 2018, The Author(s). | |
dc.publisher | Springer | |
dc.source | Unpaywall 20200831 | |
dc.subject | claudin 1 | |
dc.subject | claudin 2 | |
dc.subject | Evans blue | |
dc.subject | hemoglobin | |
dc.subject | small interfering RNA | |
dc.subject | transient receptor potential channel M4 | |
dc.subject | von Willebrand factor | |
dc.subject | enolase | |
dc.subject | fluorodeoxyglucose f 18 | |
dc.subject | messenger RNA | |
dc.subject | small interfering RNA | |
dc.subject | transient receptor potential channel M | |
dc.subject | TRPM4 protein, rat | |
dc.subject | animal experiment | |
dc.subject | animal model | |
dc.subject | animal tissue | |
dc.subject | Article | |
dc.subject | blood brain barrier | |
dc.subject | brain capillary endothelial cell | |
dc.subject | brain edema | |
dc.subject | brain infarction | |
dc.subject | brain protection | |
dc.subject | brain tissue | |
dc.subject | cell survival | |
dc.subject | cerebrovascular accident | |
dc.subject | controlled study | |
dc.subject | extravasation | |
dc.subject | hemisphere | |
dc.subject | human | |
dc.subject | human cell | |
dc.subject | in vitro study | |
dc.subject | in vivo study | |
dc.subject | infarct volume | |
dc.subject | magnetic field | |
dc.subject | male | |
dc.subject | middle cerebral artery occlusion | |
dc.subject | motor performance | |
dc.subject | multimodal imaging | |
dc.subject | nerve cell growth | |
dc.subject | neuroimaging | |
dc.subject | non invasive procedure | |
dc.subject | nonhuman | |
dc.subject | nuclear magnetic resonance imaging | |
dc.subject | positron emission tomography | |
dc.subject | priority journal | |
dc.subject | protein expression | |
dc.subject | rat | |
dc.subject | reperfusion injury | |
dc.subject | stroke patient | |
dc.subject | animal | |
dc.subject | antagonists and inhibitors | |
dc.subject | blood brain barrier | |
dc.subject | brain edema | |
dc.subject | cerebral artery disease | |
dc.subject | complication | |
dc.subject | disease model | |
dc.subject | gene expression regulation | |
dc.subject | genetics | |
dc.subject | hemispheric dominance | |
dc.subject | image processing | |
dc.subject | metabolism | |
dc.subject | microarray analysis | |
dc.subject | multimodal imaging | |
dc.subject | pathology | |
dc.subject | pathophysiology | |
dc.subject | physiology | |
dc.subject | procedures | |
dc.subject | reperfusion injury | |
dc.subject | Wistar rat | |
dc.subject | Animals | |
dc.subject | Blood-Brain Barrier | |
dc.subject | Brain Edema | |
dc.subject | Disease Models, Animal | |
dc.subject | Fluorodeoxyglucose F18 | |
dc.subject | Functional Laterality | |
dc.subject | Gene Expression Regulation | |
dc.subject | Image Processing, Computer-Assisted | |
dc.subject | Infarction, Middle Cerebral Artery | |
dc.subject | Male | |
dc.subject | Microarray Analysis | |
dc.subject | Multimodal Imaging | |
dc.subject | Phosphopyruvate Hydratase | |
dc.subject | Rats | |
dc.subject | Rats, Wistar | |
dc.subject | Reperfusion Injury | |
dc.subject | RNA, Messenger | |
dc.subject | RNA, Small Interfering | |
dc.subject | TRPM Cation Channels | |
dc.subject | von Willebrand Factor | |
dc.type | Article | |
dc.contributor.department | DEAN'S OFFICE (MEDICINE) | |
dc.contributor.department | BIOCHEMISTRY | |
dc.contributor.department | PHYSIOLOGY | |
dc.contributor.department | DUKE-NUS MEDICAL SCHOOL | |
dc.contributor.department | INSTITUTE OF MOLECULAR & CELL BIOLOGY | |
dc.contributor.department | SAW SWEE HOCK SCHOOL OF PUBLIC HEALTH | |
dc.description.doi | 10.1007/s12975-018-0621-3 | |
dc.description.sourcetitle | Translational Stroke Research | |
dc.description.volume | 10 | |
dc.description.issue | 1 | |
dc.description.page | 91-103 | |
dc.published.state | Published | |
Appears in Collections: | Elements Staff Publications |
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