P2X receptor-mediated apoptosis of human cervical epithelial cells
American Journal of Physiology - Cell Physiology, ISSN: 0363-6143, Vol: 287, Issue: 5 56-5, Page: C1349-58
2004
- 108Citations
- 47Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations108
- Citation Indexes108
- 108
- CrossRef102
- Captures47
- Readers47
- 47
Article Description
Normal human ectocervical epithelial (hECE) cells undergo apoptosis in culture. Baseline apoptosis could be increased by shifting cells to serum-free medium and blocked by lowering extracellular calcium. Treatment with the ATPase apyrase attenuated baseline apoptosis, suggesting that extracellular ATP and purinergic mechanisms control the apoptosis. Treatment with ATP and the P2X receptor analog 2′-3′-O-(4-benzoylbenzoyl)adenosine 5′-triphosphate (BzATP) increased apoptosis significantly, in a time-and dose-related manner. The threshold of ATP effect was 0.5 μM in hECE cells and ∼1 μM in CaSki cancer cells. The apoptotic effect of BzATP was additive in part to that of tumor necrosis factor (TNF)-α, and it could be attenuated by lowering extracellular calcium and by treatment with the caspase-9 inhibitor Leu-Glu-His-Asp-O-methyl-fluoromethylketone (LEHD-FMK). Treatment with BzATP activated caspase-9, and, in contrast to TNF-α, it had only a mild effect on caspase-8. Both BzATP and TNF-α activated caspase-3, suggesting that BzATP activates predominantly the mitochondrial apoptotic pathway. Both hECE and CaSki cells secrete ATP into the extracellular fluid, and mean ATP activity in conditioned medium was ∼0.5 μM, which is in the range of values that suffice to activate the P2X receptor. On the basis of these findings we propose a novel autocrine-paracrine mechanism of cervical cell apoptosis that operates by P2X receptor control of cytosolic calcium and utilizes the mitochondrial apoptotic pathway.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=6044228204&origin=inward; http://dx.doi.org/10.1152/ajpcell.00256.2004; http://www.ncbi.nlm.nih.gov/pubmed/15269006; https://journals.physiology.org/doi/10.1152/ajpcell.00256.2004; http://www.physiology.org/doi/10.1152/ajpcell.00256.2004; https://www.physiology.org/action/captchaChallenge?redirectUrl=https%3A%2F%2Fwww.physiology.org%2Fdoi%2Ffull%2F10.1152%2Fajpcell.00256.2004
American Physiological Society
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