Apoptosis of Corneal Epithelial Cells Caused by Ultraviolet B-induced Loss of K(+) is Inhibited by Ba(2.).
Apoptosis of Corneal Epithelial Cells Caused by Ultraviolet B-induced Loss of K(+) is Inhibited by Ba(2.).
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DOI：
10.1016/j.jtos.2016.05.001
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发表时间：
2016-07
期刊：
影响因子：
--
通讯作者：
Ubels JL
中科院分区：
文献类型：
--
作者：
Glupker CD;Boersma PM;Schotanus MP;Haarsma LD;Ubels JL
在室外环境水平的UVB照射下，在含有5.5 mM K+的培养基中培养的人角膜边缘上皮（HCLE）细胞会引发K+的快速损失和凋亡，但当培养基中含有泪液中存在的高浓度K+ (25 mM)时，凋亡发生的情况要少得多。由于Ba2+阻断了几个K+通道，我们测试了Ba2+敏感的K+通道是否对部分或全部uvb激活的K+丢失以及随后的caspase级联激活和凋亡负责。将培养的角膜上皮细胞暴露在80或150 mJ/cm2的UVB下。膜片钳记录用于测量uvb诱导的K+电流。对暴露于UVB的HCLE细胞进行caspase活性和TUNEL测定，然后在存在或不存在Ba2+的情况下进行孵育。uvb暴露后，HCLE细胞中的K+电流被激活。这些电流被5mm Ba2+可逆地阻断。HCLE细胞暴露于UVB后，用5 mM Ba2+孵育，caspase -9、-8和-3的激活和DNA片段化显著降低。数据证实，uvb诱导的K+电流激活和细胞内K+的丢失导致caspase级联激活和细胞凋亡。当K+通道被激活时，细胞外Ba2+通过阻止细胞内K+的丢失来抑制uvb诱导的细胞凋亡。因此，Ba2+在保护HCLE细胞免受uvb诱导的凋亡方面具有类似于细胞外K+升高的作用。这支持了我们的总体假设，即泪液中K+的升高有助于保护角膜上皮免受环境室外UVB的不利影响。
UVB exposure at ambient outdoor levels triggers rapid K+ loss and apoptosis in human corneal limbal epithelial (HCLE) cells cultured in medium containing 5.5 mM K+, but considerably less apoptosis occurs when the medium contains the high K+ concentration that is present in tears (25 mM). Since Ba2+ blocks several K+ channels, we tested whether Ba2+-sensitive K+ channels are responsible for some or all of the UVB-activated K+ loss and subsequent activation of the caspase cascade and apoptosis. Corneal epithelial cells in culture were exposed to UVB at 80 or 150 mJ/cm2. Patch-clamp recording was used to measure UVB-induced K+ currents. Caspase-activity and TUNEL assays were performed on HCLE cells exposed to UVB followed by incubation in the presence or absence of Ba2+. K+ currents were activated in HCLE cells following UVB-exposure. These currents were reversibly blocked by 5 mM Ba2+. When HCLE cells were incubated with 5 mM Ba2+ after exposure to UVB, activation of caspases-9, -8, and -3 and DNA fragmentation were significantly decreased. The data confirm that UVB-induced K+ current activation and loss of intracellular K+ leads to activation of the caspase cascade and apoptosis. Extracellular Ba2+ inhibits UVB-induced apoptosis by preventing loss of intracellular K+ when K+ channels are activated. Ba2+ therefore has effects similar to elevated extracellular K+ in protecting HCLE cells from UVB-induced apoptosis. This supports our overall hypothesis that elevated K+ in tears contributes to protection of the corneal epithelium from adverse effects of ambient outdoor UVB.
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影响因子：
3.4
作者：
Schotanus, Mark R.;Koetje, Leah R.;Ubels, John L.
通讯作者：
Ubels, John L.
DOI：
10.1111/j.1600-0420.2004.00369.x
发表时间：
2004-12-01
期刊：
ACTA OPHTHALMOLOGICA SCANDINAVICA
影响因子：
--
作者：
Podskochy, A
通讯作者：
Podskochy, A
影响因子：
--
作者：
FARRUGIA, G;RAE, J
通讯作者：
RAE, J
DOI：
10.1152/ajprenal.00471.2004
发表时间：
2005-07-01
影响因子：
4.2
作者：
Gray, DA;Frindt, G;Palmer, LG
通讯作者：
Palmer, LG
影响因子：
4.4
作者：
Gipson, IK;Spurr-Michaud, S;Russo, CL
通讯作者：
Russo, CL