| Literature DB >> 27456133 |
John R Leerar1, Courtney D Glupker1, Mark P Schotanus1, John L Ubels2.
Abstract
Exposure of human corneal limbal epithelial (HCLE) cells to UVB triggers rapid loss of K(+) and apoptosis via activation of caspases -9, -8 and -3. It has been shown that preventing loss of intracellular K(+) can inhibit apoptosis. The goal of this study was to investigate the effect of K(+) on the UVB-induced caspase activity. HCLE cells were exposed to 150 mJ/cm(2) UVB, followed by measurement of caspase activity in cell lysates. Caspase activity was measured in the presence and absence of 100 mM K(+) in the reaction buffer. UVB-induced activity of caspases -9, -8 and -3 all decreased in the presence of 100 mM K(+). These results suggest that a role of high [K(+)] in the cell is to inhibit caspase activity. Therefore, when cells lose K(+) in response to UVB, caspases are activated and cells go into apoptosis. This supports our hypothesis that K(+) inhibits caspase activity.Entities:
Keywords: Apoptosis; Caspase; Cornea; Corneal epithelium; Potassium channels; Ultraviolet
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Year: 2016 PMID: 27456133 PMCID: PMC5045793 DOI: 10.1016/j.exer.2016.07.014
Source DB: PubMed Journal: Exp Eye Res ISSN: 0014-4835 Impact factor: 3.467