| Elevated extracellular K+ inhibits apoptosis of corneal epithelial cells exposed to UV-B radiation. | |
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MedLine Citation:
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PMID: 19289117 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The goal of this study was to determine if the high [K(+)] in tears, 20-25 mM, serves to protect corneal epithelial cells from going into apoptosis after exposure to ambient UV-B radiation. Human corneal-limbal epithelial (HCLE) cells in culture were exposed to UV-B at doses of 50-200 mJ/cm(2) followed by measurement of K(+) channel activation and activity of apoptotic pathways. Patch-clamp recording showed activation of K(+) channels after UV-B exposure at 80 mJ/cm(2) or 150 mJ/cm(2) and a decrease in UV-induced K(+) efflux with increasing [K(+)](o). The UV-activated current was partially blocked by the specific K(+) channel blocker, BDS-1. DNA fragmentation, as measured by the TUNEL assay, was induced after exposure to UV-B at 100-200 mJ/cm(2). DNA fragmentation was significantly decreased when cells were incubated in 25, 50 or 100mM K(o)(+) after exposure to UV-B. The effector caspase, caspase-3, was activated by exposure to UV-B at 50-200 mJ/cm(2), but there was a significant decrease in activation when the cells were incubated in 25, 50 or 100mM K(o)(+) following exposure to UV-B. A decrease in mitochondrial potential, a possible activator of caspase-3, occurred after exposure to UV-B at 100-200 mJ/cm(2). This decrease in mitochondrial potential was prevented by 100mM K(o)(+); however, 25 or 50mM K(o)(+) provided minimal protection. Caspase-9, which is in the pathway from mitochondrial potential change to caspase-3 activation, showed little activation by UV-B radiation. Caspase-8, an initiator caspase that activates caspase-3, was activated by exposure to UV-B at 50-200 mJ/cm(2), and this UV-activation was significantly reduced by 25-100mM K(o)(+). The data show that the physiologically relevant [K(+)](o) of 25 mM can inhibit UV-B induced activation of apoptotic pathways. This suggests that the relatively high [K(+)] in tears reduces loss of K(+) from corneal epithelial cells in response to UV exposure, thereby contributing to the protection of the ocular surface from ambient UV radiation. |
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Authors:
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Katherine R Singleton; David S Will; Mark P Schotanus; Loren D Haarsma; Leah R Koetje; Susan L Bardolph; John L Ubels |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2009-03-14 |
Journal Detail:
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Title: Experimental eye research Volume: 89 ISSN: 1096-0007 ISO Abbreviation: Exp. Eye Res. Publication Date: 2009 Aug |
Date Detail:
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Created Date: 2009-07-21 Completed Date: 2009-10-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0370707 Medline TA: Exp Eye Res Country: England |
Other Details:
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Languages: eng Pagination: 140-51 Citation Subset: IM |
Affiliation:
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Department of Biology, Calvin College, Grand Rapids, MI 49546, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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physiology,
radiation effects* Caspases / metabolism Cell Line, Transformed Cells, Cultured DNA Fragmentation Dose-Response Relationship, Radiation Enzyme Activation / drug effects Epithelium, Corneal / cytology, metabolism, radiation effects* Humans In Situ Nick-End Labeling Membrane Potential, Mitochondrial / physiology, radiation effects Patch-Clamp Techniques Potassium Channels / physiology*, radiation effects Signal Transduction / radiation effects Ultraviolet Rays* |
| Grant Support | |
ID/Acronym/Agency:
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R01 EY018100/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Potassium Channels; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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