[abstract]Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores

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[abstract]Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores

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dc.contributor.author Sobolewski, P en_US
dc.contributor.author Kandel, J en_US
dc.contributor.author Klinger, AL en_US
dc.contributor.author Eckmann, DM en_US
dc.date.accessioned 2011-12-07T05:30:06Z
dc.date.available 2011-12-07T05:30:06Z
dc.date.issued 2011 en_US
dc.identifier.citation Undersea Hyperb Med. 2011 Sep-Oct;38(5) en_US
dc.identifier.isbn 1066-2936 en_US
dc.identifier.uri http://archive.rubicon-foundation.org/9470
dc.description Undersea and Hyperbaric Medicine : Journal of the Undersea and Hyperbaric Medical Society, Inc. en_US
dc.description.abstract Introduction/Background: Gas embolism is a serious complication of decompression events and certain clinical procedures, but the mechanism of resulting injury remains unclear. Previous work has demonstrated that contact between air microbubbles and endothelial cells causes a rapid intracellular calcium transient and can lead to cell death. Here, we examined the mechanism responsible for the calcium rise. Materials and methods: In each experiment, a single air microbubble (50-150 μm), trapped at the tip of a micropipette, was micromanipulated into contact with individual human umbilical vein endothelial cells (HUVECs) loaded with Fluo-4 (a fluorescent calcium indicator). Changes in intracellular calcium were then recorded via epifluorescence microscopy. In order to examine the involvement of extracellular calcium influx in the calcium rise, experiments were conducted in low-calcium buffer or with cells pre-treated with stretch activated channel blockers (gadolinium chloride or ruthenium red). The role of intracellular calcium release from endoplasmic reticulum stores was tested by pretreating cells with an IP3 receptor blocker (xestospongin C) or phospholipase C inhibitor (neomycin sulfate). Results: We confirmed that individual HUVECs rapidly respond to air bubble contact with a calcium transient. This response was markedly attenuated by use of low calcium buffer and abolished by pre-treating cells with stretch-activated channel blockers. Furthermore, the calcium response to air bubble contact depends on the release of intracellular calcium, because pretreating cells with an IP3 receptor blocker (xestospongin C) or phospholipase C inhibitor (neomycin sulfate) eliminated the response in 64% and 67% of cases, respectively. Summary/Conclusions: Collectively, our results lead us to conclude that air bubble contact with endothelial cells causes an influx of calcium through a stretch-activated channel such as a TRPV family member, triggering the release of calcium from intracellular stores via the IP3 pathway. en_US
dc.language.iso en en_US
dc.publisher Undersea and Hyperbaric Medical Society, Inc. en_US
dc.subject DISSUB en_US
dc.subject gas embolism en_US
dc.subject decompression en_US
dc.subject endothelial en_US
dc.subject HUVEC en_US
dc.subject human umbilical vein endothelial cell en_US
dc.subject calcium en_US
dc.subject IP3 receptor en_US
dc.subject xestospongin en_US
dc.subject neomycin sulfate en_US
dc.subject TRPV en_US
dc.title [abstract]Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores en_US
dc.type Article en_US

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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