Special Issue "UV-Induced Cell Death"
Quicklinks
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".
Deadline for manuscript submissions: closed (15 September 2011)
Special Issue Editor
Guest Editor
Prof. 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
Interests: cell death; photobiology; photoimmunology; skin cancer; enzymology; cell metabolism; oxidative stress; cancer metabolism; cell signalling; cytokines; inflammation; enzyme kinetics; metal oxide nanoparticles; sunscreens
Special Issue Information
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
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs).
Keywords
- ultraviolet light
- apoptosis
- necrosis
- cell membrane
- caspases
- nucleus
- signalling pathways
- enzyme activation
- autophagy
- sunburnt cell
Published Papers (6 papers)
|
Received: 14 September 2011; in revised form: 5 October 2011 / Accepted: 31 October 2011 / Published: 17 November 2011
Show/Hide Abstract
| Download PDF Full-text (708 KB) | Download XML Full-text
Abstract: In eukaryotes, DNA is compacted into a complex structure known as chromatin. The unravelling of DNA is a crucial step in DNA repair, replication, transcription and recombination as this allows access to DNA for these processes. Failure to package DNA into the nucleosome, the individual unit of chromatin, can lead to genomic instability, driving a cell into apoptosis, senescence, or cellular proliferation. Ultraviolet (UV) radiation damage causes destabilisation of chromatin integrity. UV irradiation induces DNA damage such as photolesions and subjects the chromatin to substantial rearrangements, causing the arrest of transcription forks and cell cycle arrest. Highly conserved processes known as nucleotide and base excision repair (NER and BER) then begin to repair these lesions. However, if DNA repair fails, the cell may be forced into apoptosis. The modification of various histones as well as nucleosome remodelling via ATP-dependent chromatin remodelling complexes are required not only to repair these UV-induced DNA lesions, but also for apoptosis signalling. Histone modifications and nucleosome remodelling in response to UV also lead to the recruitment of various repair and pro-apoptotic proteins. Thus, the way in which a cell responds to UV irradiation via these modifications is important in determining its fate. Failure of these DNA damage response steps can lead to cellular proliferation and oncogenic development, causing skin cancer, hence these chromatin changes are critical for a proper response to UV-induced injury.
|
|
Received: 23 August 2011; in revised form: 8 October 2011 / Accepted: 21 November 2011 / Published: 24 November 2011
Show/Hide Abstract
| Download PDF Full-text (1994 KB) | Download XML Full-text
Abstract: Ultraviolet B (UVB) induces cell death by increasing free radical production, activating apoptotic cell death pathways and depolarizing mitochondrial membrane potential. Coenzyme Q10 (CoQ10), an essential cofactor in the mitochondrial electron transport chain, serves as a potent antioxidant in the mitochondria. The aim of the present study is to establish whether CoQ10 is capable of protecting neuronal cells against UVB-induced damage. Murine hippocampal HT22 cells were treated with 0.01, 0.1 or 1 µM of CoQ10 3 or 24 h prior to the cells being exposed to UVB irradiation. The CoQ10 concentrations were maintained during irradiation and 24 h post-UVB. Cell viability was assessed by counting viable cells and MTT conversion assay. Superoxide production and mitochondrial membrane potential were measured using fluorescent probes. Levels of cleaved caspase-9, caspase-3, and apoptosis-inducing factor (AIF) were detected using immunocytochemistry and Western blotting. The results showed that UVB irradiation decreased cell viability and such damaging effect was associated with increased superoxide production, mitochondrial depolarization, and activation of caspase-9 and caspase-3. Treatment with CoQ10 at three different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide production, normalization of mitochondrial membrane potential and inhibition of caspase-9 and caspase-3 activation. It is concluded that the neuroprotective effect of CoQ10 results from inhibiting oxidative stress and blocking caspase-3 dependent cell death pathway.
|
|
Received: 16 September 2011; in revised form: 8 November 2011 / Accepted: 17 November 2011 / Published: 29 November 2011
Show/Hide Abstract
| Download PDF Full-text (2108 KB) | Download XML Full-text
Abstract: When a replicative DNA polymerase stalls upon encountering a photoproduct on the template strand, it is relieved by other low-processivity polymerase(s), which insert nucleotide(s) opposite the lesion. Using an alkaline sucrose density gradient sedimentation technique, we previously classified this process termed UV-induced translesion replication (UV-TLS) into two types. In human cancer cells or xeroderma pigmentosum variant (XP-V) cells, UV-TLS was inhibited by caffeine or proteasome inhibitors. However, in normal human cells, the process was insensitive to these reagents. Reportedly, in yeast or mammalian cells, REV3 protein (a catalytic subunit of DNA polymerase ζ) is predominantly involved in the former type of TLS. Here, we studied UV-TLS in fibroblasts derived from the Rev3-knockout mouse embryo (Rev3KO-MEF). In the wild-type MEF, UV-TLS was slow (similar to that of human cancer cells or XP-V cells), and was abolished by caffeine or MG-262. In 2 cell lines of Rev3KO-MEF (Rev3−/− p53−/−), UV-TLS was not observed. In p53KO-MEF, which is a strict control for Rev3KO-MEF, the UV-TLS response was similar to that of the wild-type. Introduction of the Rev3 expression plasmid into Rev3KO-MEF restored the UV-TLS response in selected stable transformants. In some transformants, viability to UV was the same as that in the wild-type, and the death rate was increased by caffeine. Our findings indicate that REV3 is predominantly involved in UV-TLS in mouse cells, and that the REV3 translesion pathway is suppressed by caffeine or proteasome inhibitors.
|
|
Received: 11 October 2011; in revised form: 15 November 2011 / Accepted: 30 November 2011 / Published: 6 December 2011
Show/Hide Abstract
| Download PDF Full-text (327 KB) | Download XML Full-text
Abstract: The E2F transcription factor family is traditionally associated with cell cycle control. However, recent data has shown that activating E2Fs (E2F1-3a) are potent activators of apoptosis. In contrast, the recently cloned inhibitory E2Fs (E2F7 and 8) appear to antagonize E2F-induced cell death. In this review we will discuss (i) the potential role of E2Fs in UV-induced cell death and (ii) the implications of this to the development of UV-induced cutaneous malignancies.
|
|
Received: 20 November 2011; in revised form: 14 December 2011 / Accepted: 16 December 2011 / Published: 23 December 2011
Show/Hide Abstract
| Download PDF Full-text (429 KB) | Download XML Full-text
Abstract: Solar ultraviolet (UV) radiation is an important environmental factor that leads to immune suppression, inflammation, photoaging, and skin carcinogenesis. Here, we reviewed the specific signal transduction pathways and transcription factors involved in the cellular response to UV-irradiation. Increasing experimental data supporting a role for p38, MAPK, JNK, ERK1/2, and ATM kinases in the response network to UV exposure is discussed. We also reviewed the participation of NF-κB, AP-1, and NRF2 transcription factors in the control of gene expression after UV-irradiation. In addition, we discussed the promising chemotherapeutic intervention of transcription factors signaling by natural compounds. Finally, we focused on the review of data emerging from the use of DNA microarray technology to determine changes in global gene expression in keratinocytes and melanocytes in response to UV treatment. Efforts to obtain a comprehensive portrait of the transcriptional events regulating photodamage of intact human epidermis after UV exposure reveals the existence of novel factors participating in UV-induced cell death. Progress in understanding the multitude of mechanisms induced by UV-irradiation could lead to the potential use of protein kinases and novel proteins as specific targets for the prevention and control of skin cancer.
|
|
Received: 1 February 2012; in revised form: 5 March 2012 / Accepted: 16 March 2012 / Published: 5 April 2012
Show/Hide Abstract
| Download PDF Full-text (466 KB) | Download XML Full-text
Abstract: Ultraviolet C (UVC) is a DNA damage inducer, and 20 J/m2 of UVC irradiation caused cell growth inhibition and induced cell death after exposure for 24–36 h. The growth of NIH 3T3 cells was significantly suppressed at 24 h after UVC irradiation whereas the proliferation of A431 cells was inhibited until 36 h after UVC irradiation. UVC irradiation 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 1–12 h after UVC irradiation and increased again at 24 h in both cell lines. 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 secretion from NIH 3T3 cells and A431 cells were similar despite the differential profile in UVC-induced COX-2 up-regulation. Besides, COX-2 might play different roles in cellular response to UVC irradiation in various cell lines.
|
Last update: 26 September 2012
