Special Issue "UV-Induced Cell Death"

Guest Editor
Dr. Terrence Piva
RMIT University, PO Box 71, Bundoora, Victoria 3083, Australia
Website: http://www.rmit.edu.au/browse;ID=kn6c15nk6ilu
E-Mail: terry.piva@rmit.edu.au
Phone: Office +61-3-9925 6503; Lab 9925 7278
Fax: +61-3-9925 7063

Dear Colleagues,

When we think of UV radiation we imagine getting a suntan, and sometimes when we are in the sun too long we end up getting sunburnt.  Sunburnt skin cells are those, which undergo apoptosis as a result of UV exposure.  Other cells in the skin can undergo necrosis.  The mechanisms by which UVA, UVB and UVC trigger cell death in different cells differs depending on the cell line examined and the dose and type of UV that is used.  This issue will look at the effects UV radiation has on cell death, looking at but not restricted to changes in the activity of intracellular signalling pathways, caspase activation, membrane damage, production of ROS or via direct nuclear damage and the effect this has on the cell as it dies.  An often asked question is “does a cell undergoing apoptosis release molecules which may influence those around it”, hopefully this issue may help shed light on this question.  For instance does a dying cell release enzymes of growth factors, which may stimulate adjacent cells to undergo cell division to replace lost cells?  It is unclear if this occurs in the skin when cells are exposed to too much sunlight.  I encourage you to submit a manuscript to this issue and help shed further “light” on the lethal effects UV radiation have on cells.

Prof. Dr. Terrence Piva
Guest Editor

Submission

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• ultraviolet light
• apoptosis
• necrosis
• cell membrane
• caspases
• nucleus
• signalling pathways
• enzyme activation
• autophagy
• sunburnt cell

Title: UV Induced Cytotoxicity: Development of in vitro Phototoxicity Assays in the NCTC 2544 Keratinocyte Cell Line and ex vivo Human Skin
Authors: Astrid A. Reus ¹, Saertje Verkoeijen ², Johanna Louter-van de Haar ² and Cyrille A.M. Krul ^2,3
Afiliations: ¹ TNO Triskelion BV, Utrechtseweg 48, 3704 HE Zeist, The Netherlands; E-Mail: astrid.reus@tno.triskelion.nl
² University of Applied Sciences Utrecht, F.C. Dondersstraat 65, 3572 JE Utrecht, The Netherlands
³ TNO Healthy Living, Utrechtseweg 48, 3704 HE, Zeist, The Netherlands
Abstract: Solar UV radiation can activate exogenous compounds that reach the skin, such as ingredients of personal care products and pharmaceuticals. Activation may result in adverse effects such as erythema and photo-induced ageing of the skin. The in vitro 3T3 neutral red uptake assay is currently the only validated assay for photosafety assessment of exogenous compounds that reach the skin. However, this assay recently raised concerns about oversensitivity (overprediction of phototoxicity). Since the relevance of positive results of in vitro phototoxicity tests needs to be confirmed in vivo, this consequently results in unnecessary costly and time consuming in vivo testing or abandoned compounds. Because the molecular mechanism of UV-induced toxicity, such as photogenotoxicity and photoirritation, are the same, phototoxicity tests that predict the effects in humans are important and urgently needed. For these reasons in vitro phototoxicity assays using the human keratinocyte cell line NCTC 2544 and ex vivo human skin obtained from surgery were developed. Ex vivo human skin has the advantage of mimicking realistic exposure conditions due to its barrier function of the stratum corneum, human origin and possibility to measure effects in the target organ for photoirritation. Preliminary results and points to consider for further validation will be discussed.

Title: The Increased Activity of Cell Surface Metallopeptidase Activity in HeLa Cells Undergoing UV-Induced Apoptosis is not Mediated by Caspase 3
Authors: Terrence Piva et al.
Affiliation: School of Medical Sciences, College of Science, Engineering & Health, RMIT University, BUNDOORA  Vic 3083, Australia; E-Mail: terry.piva@rmit.edu.au
Abstract: We have previously shown that in HeLa cells treated with a variety of agents that there is an increase in cell surface metallopeptidase activity in those cells undergoing apoptosis (Piva et al., 1999).  The increase in metallopepetidase activity observed in cells undergoing apoptosis was not inhibited when the cells were exposed to the aminopeptidase inhibitor bestatin, the matrix metalloprotease inhibitor BB3103 or the caspase 3 inhibitor DEVD.  However when the cells were treated with the PARP inhibitor 3-aminobenzamide, there was no increase in cell surface peptidase activity in the apoptotic cell population.  There was no difference between the apoptotic cells of the treated cultures when observed under electron microscopy.  The apoptotic cells were all found to have similar profiles of phosphatidylserine eversion on the cell membrane, as well as the cleavage of PARP and actin.  The results suggests that other caspases apart from caspase 3 can cleave PARP in these cells.  Caspase 3 activity was similar in the treated cell populations except where it was inhibited in the presence of DEVD.  The increase in cell surface metallopepetidase activity in cells undergoing apoptosis is not due to increased either caspase 3 activity or the cleavage of PARP or actin, but arises from another mechanism.

Title: Ultraviolet C Irradiation Induces Different Expression of Cyclooxygenase 2 in NIH 3T3 cells and A431 Cells: the Roles of COX-2 are Different in Various Cell Lines
Authors: Ming-Hong Tai ¹, Chien-Hui Weng ², Dir-Pu Mon ³, Chun-Yi Hu ^3,4 and Ming-Hsiu Wu ^3,4
Affiliations: ¹ Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan
² Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan
³ Department of Nutrition and Health Science, Fooyin University, Kaohsiung County, Taiwan; E-Mail: mt116@mail.fy.edu.tw
⁴ Research Center of Health Food, Fooyin University, Kaohsiung County, Taiwan
Abstract: Ultraviolet C (UVC) is a DNA damage inducer, and UVC irradiation (20 J/m²) caused cell growth inhibition and induced cell death after exposure for 24-36 h. The growth of NIH 3T3 cells was promptly suppressed by UVC irradiation whereas the proliferation of A431 cells was not immediately inhibited by UVC irradiation. UVC increased COX-2 expression and such up-regulation reached a maximum during 3-6 h in NIH 3T3 cells. In contrast, UVC-induced COX-2 reached a maximum after 24-36 h in A431 cells. Measuring prostaglandin E2 (PGE2) level showed a biphasic profile that PGE2 release was rapidly elevated in 3-6 h after UVC irradiation and increased again at 24-36 h. Treatment with the selective COX-2 inhibitor, SC 791, during maximum expression of COX-2 induction, attenuated the UVC induced-growth inhibition in NIH 3T3 cells. In contrast, SC 791 treatment after UVC irradiation enhanced death of A431 cells. These data showed that the patterns of UVC-induced PGE2 secretions from NIH 3T3 cells and A431 cells were very similar, while the profiles of COX-2 up-regulation by UVC were different in these two cell lines, and implied that COX-2 might play different roles in cellular response to UVC irradiation in various cell lines.
Keywords: ultraviolet C (UVC), cyclooxygenases-2 (COX-2), prostaglandin E2 (PGE2), nucleophosmin/B23 (NPM/B23), NIH 3T3 cells, A431 cells