UV-Induced Corneal Epithelial Cell Death by Activation of Potassium Channels

Wang, Ling; Li, Tie; Luo, Lu

doi:10.1167/iovs.03-0590

Cited by 42 publications

(50 citation statements)

References 35 publications

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“…(Soliven et al, 1991;Dubois and Rouzaire-Dubois, 1993;Bright et al, 1994;Duprat et al, 1995;Szabo et al, 1996;Wang et al, 1999a,b;Lu et al, 2003;Gao et al, 2004;Guo et al, 2005). For example, we, as well as other researchers, have shown that stimulation of K + channel activity and dramatic loss of intracellular K + can result in apoptosis in the corneal epithelium, neurons, myeloblastic ML-1 cells, and other cell types (Schulz et al, 1996;Eldadah et al, 1997;Yu et al, 1997;Wang et al, 1999aWang et al, ,2003Lu et al, 2003;Trimarchi et al, 2002;Remillard and Yuan, 2004). It seems that there are dual functions of K + channels involving cell proliferation regulated by epidermal growth factor (EGF) (Lu et al, 2001a) and playing a role in mediating cell death induced by UV irradiation (Wang et al, 1999aLu et al, 2003).…”

Section: Introductionmentioning

confidence: 68%

“…Each of these responses is dependent on K + channel activation. Therefore, corneal epithelial renewal, which is a result of a balance between cell proliferation, apoptosis and differentiation, is dependent on K + channel activation by stimuli that affect each of these responses Wang et al, 2003). There is one type of K + channels in corneal epithelial cells with characteristics similar to Kv3.4 channels.…”

Section: Expression Of Kv Channels In Corneal Epithelial Cellsmentioning

confidence: 99%

“…However, there is currently very little information regarding how UV irradiation induces corneal epithelial cell apoptosis (Lu et al, 2001b). Recent studies provide cellular and molecular mechanisms involving hyperactivation of a K + channel in corneal epithelial cells Wang et al, 2003). Data from earlier studies of our lab and others show that blocking K + efflux by a K + channel blocker or by increasing extracellular K + inhibited apoptosis in human eosinophil, human myeloid cells and mouse cortical neurons (McCarthy et al, 1994;Beauvais et al, 1995b;Kaneko et al, 1999).…”

Section: Uv Irradiation-induced K + Channel Hyperactivitymentioning

confidence: 99%

“…In addition, various techniques, including DNA fragmentation, nuclear staining, caspase 3 activation and TUNEL assay, are used to detect UV-induced apoptosis in the corneal epithelium Wang et al, 2003). For example, H-E staining revealed a normal corneal epithelial histological structure in cultured rat corneas (Fig.…”

Section: Kv Channel Mediating Uv-induced Apoptosismentioning

confidence: 99%

“…In many different cell types, UV irradiation can induce increases in the activity of two other limbs of the MAP kinase signaling cascade: ERK and p38 (Radler-Pohl et al, 1993;Li et al, 2002;Wang et al, 2003). Exposure of corneal epithelial cells to UV irradiation also induces activation of the ERK limb.…”

Section: Dependence Of Uv-induced Erk or P38 Activation On K + Channementioning

confidence: 99%

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Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

2006

Progress in Retinal and Eye Research

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One of the functional roles of the corneal epithelial layer is to protect the cornea, lens and other underlying ocular structures from damages caused by environmental insults. It is important for corneal epithelial cells to maintain this function by undergoing continuous renewal through a dynamic process of wound healing. Previous studies in corneal epithelial cells have provided substantial evidence showing that environmental insults, such as ultraviolet (UV) irradiation and other biohazards, can induce stress-related cellular responses resulting in apoptosis and thus interrupt the dynamic process of wound healing. We found that UV irradiation-induced apoptotic effects in corneal epithelial cells are started by the hyperactivation of K + channels in the cell membrane resulting in a fast loss of intracellular K + ions. Recent studies provide further evidence indicating that these complex responses in corneal epithelial cells are resulted from the activation of stressrelated signaling pathways mediated by K + channel activity. The effect of UV irradiation on corneal epithelial cell fate shares common signaling mechanisms involving the activation of intracellular responses that are often activated by the stimulation of various cytokines. One piece of evidence for making this distinction is that at early times UV irradiation activates a Kv3.4 channel in corneal epithelial cells to elicit activation of c-Jun N-terminal kinase cascades and p53 activation leading to cell cycle arrest and apoptosis. The hypothetic model is that UV-induced potassium channel hyperactivity as an early event initiates fast cell shrinkages due to the loss of intracellular potassium, resulting in the activation of scaffolding protein kinases and cytoskeleton reorganizations. This review article presents important control mechanisms that determine Kv channel activity-mediated cellular responses in corneal epithelial cells, involving activation of stress-induced signaling pathways, arrests of cell cycle progression and/or induction of apoptosis.

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