Please use this identifier to cite or link to this item: https://doi.org/10.1007/s00424-013-1347-4
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dc.titleTRPM4 inhibition promotes angiogenesis after ischemic stroke
dc.contributor.authorLoh, K.P.
dc.contributor.authorNg, G.
dc.contributor.authorYu, C.Y.
dc.contributor.authorFhu, C.K.
dc.contributor.authorYu, D.
dc.contributor.authorVennekens, R.
dc.contributor.authorNilius, B.
dc.contributor.authorSoong, T.W.
dc.contributor.authorLiao, P.
dc.date.accessioned2014-11-26T07:49:14Z
dc.date.available2014-11-26T07:49:14Z
dc.date.issued2014-03
dc.identifier.citationLoh, K.P., Ng, G., Yu, C.Y., Fhu, C.K., Yu, D., Vennekens, R., Nilius, B., Soong, T.W., Liao, P. (2014-03). TRPM4 inhibition promotes angiogenesis after ischemic stroke. Pflugers Archiv European Journal of Physiology 466 (3) : 563-576. ScholarBank@NUS Repository. https://doi.org/10.1007/s00424-013-1347-4
dc.identifier.issn00316768
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/109719
dc.description.abstractTransient receptor potential melastatin 4 (TRPM4) is a voltage-dependent, nonselective cation channel. Under pathological conditions, sustained activation of TRPM4 leads to oncotic cell death. Here, we report the upregulation of TRPM4 in vascular endothelium following hypoxia/ischemia in vitro and in vivo. In human umbilical vein endothelial cells, TRPM4 expression was increased at both the mRNA and protein levels following oxygen-glucose deprivation. Blocking TRPM4 with 9-phenanthrol greatly enhanced tube formation on Matrigel. In a rat permanent middle cerebral artery occlusion model, TRPM4 was upregulated in the vascular endothelium within the penumbra region after stroke. TRPM4 expression peaked 1 day post-occlusion and gradually decreased. In vivo siRNA-mediated TRPM4 silencing enhanced angiogenesis and improved capillary integrity. A twofold reduction in infarct volume and a substantial recovery of motor function were observed in animals receiving the siRNA treatment. Interestingly, the protective effect of TRPM4 suppression disappeared 5 days after stroke induction, indicating that TRPM4 upregulation is critical for cerebral damage during the acute phase of stroke. TRPM4 could be a potential therapeutic target for ischemic stroke. © 2013 Springer-Verlag Berlin Heidelberg.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1007/s00424-013-1347-4
dc.sourceScopus
dc.subjectAngiogenesis
dc.subjectCapillary integrity
dc.subjectIschemic stroke
dc.subjectTRPM4 channel
dc.typeArticle
dc.contributor.departmentPHYSIOLOGY
dc.description.doi10.1007/s00424-013-1347-4
dc.description.sourcetitlePflugers Archiv European Journal of Physiology
dc.description.volume466
dc.description.issue3
dc.description.page563-576
dc.description.codenPFLAB
dc.identifier.isiut000331719400019
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