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|Title:||TRPM4 inhibition promotes angiogenesis after ischemic stroke||Authors:||Loh, K.P.
|Issue Date:||Mar-2014||Citation:||Loh, 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||Abstract:||Transient 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.||Source Title:||Pflugers Archiv European Journal of Physiology||URI:||http://scholarbank.nus.edu.sg/handle/10635/109719||ISSN:||00316768||DOI:||10.1007/s00424-013-1347-4|
|Appears in Collections:||Staff Publications|
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