ArticleAmerican journal of physiology. Cell physiology2011
Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction.European journal of applied physiology · 2017Trial
- Alteration of Essential Cell Function by Ultrasound-Targeted Microbubble Cavitation.Current cardiology reports · 2025Review
- Biohybrid lung Development: Towards Complete Endothelialization of an Assembled Extracorporeal Membrane Oxygenator.Bioengineering (Basel, Switzerland) · 2023Article
- Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.Frontiers in immunology · 2023Review
- Cell viability assessment associated with a contact of gas bubbles produced by femtosecond laser breakdown in cell culture media.Scientific reports · 2022Article
- Expansion and differentiation of ex vivo cultured erythroblasts in scalable stirred bioreactors.Biotechnology and bioengineering · 2022Article
- Full-Face Mask Use during SCUBA Diving Counters Related Oxidative Stress and Endothelial Dysfunction.International journal of environmental research and public health · 2022Article
- Endothelial Injury in Diving: Atomic Force-, Electronic-, and Light-Microscopy Study of the Ovine Decompressed Blood Vessels.Frontiers in physiology · 2021Article
- Simulated air dives induce superoxide, nitric oxide, peroxynitrite, and CaJournal of physiology and biochemistry · 2020Article
- Biphasic effects of autophagy on decompression bubble-induced endothelial injury.Journal of cellular and molecular medicine · 2019Article
- The Blockade of Store-Operated Calcium Channels Improves Decompression Sickness in Rats.Frontiers in physiology · 2019Article
- Acute decompression following simulated dive conditions alters mitochondrial respiration and motility.American journal of physiology. Cell physiology · 2018Article
- Spatial-Temporal Cellular Bioeffects from Acoustic Droplet Vaporization.Theranostics · 2018Article
- Quantification of cell-bubble interactions in a 3D engineered tissue phantom.Scientific reports · 2017Article
- The answer is blowing in the wind: an uncommon cause for severe ARDS accompanied by circulatory insufficiency requiring extracorporeal membrane oxygenation.BMJ case reports · 2017Article
- Nanobubbles Form at Active Hydrophobic Spots on the Luminal Aspect of Blood Vessels: Consequences for Decompression Illness in Diving and Possible Implications for Autoimmune Disease-An Overview.Frontiers in physiology · 2017Review
- Article
- Automated detection of whole-cell mitochondrial motility and its dependence on cytoarchitectural integrity.Biotechnology and bioengineering · 2015Article
- Chemically grafted fibronectin for use in QCM-D cell studies.Biosensors & bioelectronics · 2014Article
- Pefluorocarbon inhibition of bubble induced Ca2+ transients in an in vitro model of vascular gas embolism.Experimental biology and medicine (Maywood, N.J.) · 2014Article
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Authors and funding
4 authors.
Funding
Abstract
Gas embolism is a serious complication of decompression events and 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. Single air microbubbles (50-150 μm), trapped at the tip of a micropipette, were 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. First, we confirmed that HUVECs rapidly respond to air bubble contact with a calcium transient. Next, we examined the involvement of extracellular calcium influx by conducting experiments in low calcium buffer, which markedly attenuated the response, or by pretreating cells with stretch-activated channel blockers (gadolinium chloride or ruthenium red), which abolished the response. Finally, we tested the role of intracellular calcium release by pretreating cells with an inositol 1,4,5-trisphosphate (IP3) receptor blocker (xestospongin C) or phospholipase C inhibitor (neomycin sulfate), which eliminated the response in 64% and 67% of cases, respectively. 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 transient receptor potential vanilloid family member, triggering the release of calcium from intracellular stores via the IP3 pathway.
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