[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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Title: [abstract]Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores
Author: Sobolewski, P; Kandel, J; Klinger, AL; Eckmann, DM
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.
Description: Undersea and Hyperbaric Medicine : Journal of the Undersea and Hyperbaric Medical Society, Inc.
URI: http://archive.rubicon-foundation.org/9470
Date: 2011

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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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