ArticleThe Journal of membrane biology2004
Formation of transient non-protein calcium pores by lysophospholipids in S49 Lymphoma cells.
Article in The Journal of membrane biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Differential effects of lysophospholipid headgroups, acyl chain length and saturation on vacuole acidification, CaFrontiers in cell and developmental biology · 2026Article
- Phosphatidylethanolamine homeostasis under conditions of impaired CDP-ethanolamine pathway or phosphatidylserine decarboxylation.Frontiers in nutrition · 2022Review
- Effects of Subretinal Gene Transfer at Different Time Points in a Mouse Model of Retinal Degeneration.PloS one · 2016Article
- Dopaminergic Neurons Respond to Iron-Induced Oxidative Stress by Modulating Lipid Acylation and Deacylation Cycles.PloS one · 2015Article
- AAV-mediated lysophosphatidylcholine acyltransferase 1 (Lpcat1) gene replacement therapy rescues retinal degeneration in rd11 mice.Investigative ophthalmology & visual science · 2014Article
- Poxvirus membrane biogenesis: rupture not disruption.Cellular microbiology · 2013Review
- Relationship between membrane permeability and specificity of human secretory phospholipase A(2) isoforms during cell death.Biochimica et biophysica acta · 2011Article
- Loss of lysophosphatidylcholine acyltransferase 1 leads to photoreceptor degeneration in rd11 mice.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Modulation of the cold-activated channel TRPM8 by lysophospholipids and polyunsaturated fatty acids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Mechanism of lysophosphatidylcholine-induced lysosome destabilization.The Journal of membrane biology · 2007Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Palmitoyl-lysophosphatidylcholine promotes a transient calcium influx in lymphoma cells. Previously, it was observed that this influx was accompanied by a temporary increase in propidium iodide permeability that appeared linked to calcium entry. Those studies demonstrated that cobalt or nickel could block the response to lysophosphatidylcholine and raised the question of whether the calcium conductance involved specific channels. This communication describes a series of experiments to address that issue. The time dependence and structural specificity of the responses to lysophosphatidylcholine reinforced the hypothesis of a specific channel or transporter. Nevertheless, observations using patch clamp or calcium channel blockers suggested that this "channel" does not involve proteins. Alternative protein-mediated mechanisms such as indirect involvement of the sodium-calcium exchanger and the sodium-potassium ATPase were also excluded. Experiments with extracellular and intracellular calcium chelators suggested a common route of entry for calcium and propidium iodide. More directly, the ability of lysophosphatidylcholine to produce cobalt-sensitive permeability to propidium iodide was reproduced in protein-free artificial membranes. Finally, the transient nature of the calcium time course was rationalized quantitatively by the kinetics of lysophosphatidylcholine metabolism. These results suggest that physiological concentrations of lysophosphatidylcholine can directly produce membrane pores that mimic some of the properties of specific protein channels.
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