ArticleNaunyn-Schmiedeberg's archives of pharmacology2004
Epigallocatechin-3-gallate increases intracellular [Ca2+] in U87 cells mainly by influx of extracellular Ca2+ and partly by release of intracellular stores.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- A Comprehensive Review on Beneficial Effects of Catechins on Secondary Mitochondrial Diseases.International journal of molecular sciences · 2022Review
- Article
- Suppressive Effects ofFrontiers in pharmacology · 2018Article
- Natural products induce a G protein-mediated calcium pathway activating p53 in cancer cells.Toxicology and applied pharmacology · 2015Article
- Inhibition of the intracellular Ca(2+) transporter SERCA (Sarco-Endoplasmic Reticulum Ca(2+)-ATPase) by the natural polyphenol epigallocatechin-3-gallate.Journal of bioenergetics and biomembranes · 2012Article
- Trivanillic polyphenols with anticancer cytostatic effects through the targeting of multiple kinases and intracellular Ca2+ release.Journal of cellular and molecular medicine · 2012Article
- Apigenin, a plant-derived flavone, activates transient receptor potential vanilloid 4 cation channel.British journal of pharmacology · 2012Article
- Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications.Biochemical pharmacology · 2011Review
- Epigallocatechin-3-gallate has dual, independent effects on the cardiac sarcoplasmic reticulum/endoplasmic reticulum Ca2+ ATPase.Journal of muscle research and cell motility · 2011Article
- Grape seed proanthocyanidin extract inhibits glutamate-induced cell death through inhibition of calcium signals and nitric oxide formation in cultured rat hippocampal neurons.BMC neuroscience · 2011Article
- Green tea catechins are potent sensitizers of ryanodine receptor type 1 (RyR1).Biochemical pharmacology · 2010Article
- Octyl Gallate Inhibits ATP-induced Intracellular Calcium Increase in PC12 Cells by Inhibiting Multiple Pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010Article
- Elucidation of susceptible factors to endoplasmic reticulum stress-mediated anticancer activity in human hepatocellular carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- Inhibition of Helicobacter pylori and associated urease by oregano and cranberry phytochemical synergies.Applied and environmental microbiology · 2005Article
- Editorial guidelines for manuscripts on the pharmacology of plant extracts.Naunyn-Schmiedeberg's archives of pharmacology · 2005Article
- (-)-Epigallocatechin-3-gallate induces contraction of the rat aorta by a calcium influx-dependent mechanism.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Green tea has been receiving considerable attention as a possible preventive agent against cancer and cardiovascular disease. Epigallocatechin-3-gallate (EGCG) is a major polyphenol component of green tea. Using digital calcium imaging and an assay for [3H]-inositol phosphates, we determined whether EGCG increases intracellular [Ca2+] ([Ca2+]i) in non-excitable human astrocytoma U87 cells. EGCG induced concentration-dependent increases in [Ca2+]i. The EGCG-induced [Ca2+]i increases were reduced to 20.9% of control by removal of extracellular Ca2+. The increases were also inhibited markedly by treatment with the non-specific Ca2+ channel inhibitors cobalt (3 mM) for 3 min and lanthanum (1 mM) for 5 min. The increases were not significantly inhibited by treatment for 10 min with the L-type Ca2+ channel blocker nifedipine (100 nM). Treatment with the inhibitor of endoplasmic reticulum Ca2+-ATPase thapsigargin (1 micro M) also significantly inhibited the EGCG-induced [Ca2+]i increases. Treatment for 15 min with the phospholipase C (PLC) inhibitor neomycin (300 micro M) attenuated the increases significantly, while the tyrosine kinase inhibitor genistein (30 micro M) had no effect. EGCG increased [3H]-inositol phosphates formation via PLC activation. Treatment for 10 min with mefenamic acid (100 micro M) and flufenamic acid (100 micro M), derivatives of diphenylamine-2-carboxylate, blocked the EGCG-induced [Ca2+]i increase in non-treated and thapsigargin-treated cells but indomethacin (100 micro M) did not affect the increases. Collectively, these data suggest that EGCG increases [Ca2+]i in non-excitable U87 cells mainly by eliciting influx of extracellular Ca2+ and partly by mobilizing intracellular Ca2+ stores by PLC activation. The EGCG-induced [Ca2+]i influx is mediated mainly through channels sensitive to diphenylamine-2-carboxylate derivatives.
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