Ultraviolet radiation-induced apoptosis in keratinocytes: On the role of cytosolic factors

Assefa, Zerihun; Laethem, An Van; Garmyn, Marjan; Agostinis, Patrizia

doi:10.1016/j.bbcan.2005.04.001

Cited by 145 publications

(185 citation statements)

References 128 publications

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“…We previously showed that exposure of the adult C. elegans germ line to IR results in cell cycle arrest in the mitotic stem cell compartment and apoptotic death of pachytene cells. 18 To determine the effects of UV light on germline physiology, which causes a pattern of DNA damage distinct from the one observed following IR, 11 we exposed young adult hermaphrodites to increasing doses of UV-C radiation (254 nm) and measured the extent of germ cell apoptosis ( Figure 1) and cell cycle arrest (see below) over time. We found that UV-C induces germ cell death in a dosedependent manner, reaching a plateau at 100 J/m 2 ( Figure 1a).…”

Section: Resultsmentioning

confidence: 99%

“…1,10 Ultraviolet (UV) light in the UV-B (o280 nm) and UV-C (280-315 nm) range damages DNA through the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4 PPs). 11,12 UV radiation is a potent mutagen and both epidemiological and molecular evidence have established it as the major cause of human skin cancers. The removal of UV-induced DNA lesions is undertaken by the nucleotide excision repair (NER) machinery, which also removes adducts produced by chemotherapeutic agents, such as cisplatin.…”

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confidence: 99%

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The nucleotide excision repair pathway is required for UV-C-induced apoptosis in Caenorhabditis elegans

et al. 2007

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Ultraviolet (UV) radiation is a mutagen of major clinical importance in humans. UV-induced damage activates multiple signaling pathways, which initiate DNA repair, cell cycle arrest and apoptosis. To better understand these pathways, we studied the responses to UV-C light (254 nm) of germ cells in Caenorhabditis elegans. We found that UV activates the same cellular responses in worms as in mammalian cells. Both UV-induced apoptosis and cell cycle arrest were completely dependent on the p53 homolog CEP-1, the checkpoint proteins HUS-1 and CLK-2, and the checkpoint kinases CHK-2 and ATL-1 (the C. elegans homolog of ataxia telangiectasia and Rad3-related); ATM-1 (ataxia telangiectasia mutated-1) was also required, but only at low irradiation doses. Importantly, mutation of genes encoding nucleotide excision repair pathway components severely disrupted both apoptosis and cell cycle arrest, suggesting that these genes not only participate in repair, but also signal the presence of damage to downstream components of the UV response pathway that we delineate here. Our study suggests that whereas DNA damage response pathways are conserved in metazoans in their general outline, there is significant evolution in the relative importance of individual checkpoint genes in the response to specific types of DNA damage.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

The nucleotide excision repair pathway is required for UV-C-induced apoptosis in Caenorhabditis elegans

et al. 2007

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“…Bcl-XL protein is expressed in the upper layer of the epidermis (Krajevski, 1994) and it was shown to protect KCs against UV-B-induced cell death and against the formation of skin tumours in transgenic mice (Assefa et al, 2005). Its overexpression in human KCs blocked the UV-B-induced apoptosis both in vivo and in vitro (Takahashi, 2001) and acted as antioxidant and inhibitor of ROS generation (Hockenbery et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…It causes alterations in the skin appearance, such as erythema, sunburn, hyper-pigmentation, photoaging or hyperplasia, immune suppression and DNA damage, which jointly can contribute to skin cancer induction (InYoung and Yu-Ying, 2014). UVR is a full carcinogen, being able to damage molecules (nucleic acids, proteins, lipids, saccharides) directly or indirectly through ROS production (Assefa et al, 2005). However, neither the source nor the pathways of these molecules generation after UVR are clearly understood.…”

Section: Morphology Analysismentioning

confidence: 99%

Modulation of the UV-B-induced Oxidative Stress and Apoptosis in HaCaT Cell Line with <i>Calluna vulgaris</i> Extract

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et al. 2015

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The reactive oxygen species (ROS) production due to ultraviolet B (UV-B) exposure is extremely harmful to the skin. It causes lesions of DNA, proteins and lipids and leads to cellular death. In the present study the UV-B-induced ROS and subsequent apoptosis in the human keratinocyte cell line (HaCaT) were counterbalanced by a plant extract with antioxidant capacity. Some molecules modulated by common heather (Calluna vulgaris) (CV) extract through which this may exert its photoprotective effects were also identified. The ROS were evaluated with CM-H2DCFDA assay, while apoptosis and Bax-α/Bcl-xL molecules with ELISA. The extract was standardized according to its polyphenolic content and the most important biologically active compounds, such as hyperozid, quercetin, isoquercetin, kampferol were evidenced by high-performance liquid chromatography. The UV-B induced ROS production occurred at its highest level at 2 h after the exposure of the HaCaT cells, while apoptosis later, at 4 h. The most significant changes in Bax-α and Bcl-XL proteins induced by UV-B, as well as the highest effect of the extract on apoptosis, were both registered at 4 h. The CV extract decreased concentration-and time-dependently the UV-B-induced ROS production and prevented apoptosis. These effects of CV occurred, at least to a certain extent, due to the modulation of Bax-α/Bcl-XL proteins. These findings suggest that skin cells could be protected from some of the UV-B-induced harmful effects by the administration of the CV extract, which may be further exploited as a potential photoprotective agent.

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“…Evidence also suggests that severely UVB-damaged cells undergo apoptosis in favor of surrounding normal cells. Accordingly, UVB-mediated apoptosis is currently regarded as a protective mechanism preventing malignant transformation by eliminating cells that carry high loads of UVB-induced DNA damage (3,7).…”

Section: Introductionmentioning

confidence: 99%

Reduced ultraviolet-induced DNA damage and apoptosis in human skin with topical application of a photolyase-containing DNA repair enzyme cream: Clues to skin cancer prevention

et al. 2011

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Abstract. The exposure of human skin to ultraviolet radiation (UVR) results in the formation of DNA photolesions that give rise to photoaging, mutations, cell death and the onset of carcinogenic events. Photolyase (EC 4.1.99.3) is a DNA repair enzyme that reverses damage caused by exposure to UVR. We sought to investigate whether addition of photolyase enhances the protection provided by a traditional sunscreen (SS), by reducing the in vivo formation of cyclobutane-type pyrimidine dimers (CPDs) and UVR-induced apoptosis in human skin. Ten volunteers (Fitzpatrick skin type II) were exposed to solar-simulated (ss) UVR at a three times minimal erythema dose for 4 consecutive days. Thirty minutes prior to each exposure, the test materials [vehicle, SS (sun protection factor 50) alone, and SS plus photolyase from Anacystis nidulans] were applied topically to three different sites. One additional site was left untreated and one received ssUVR only. Biopsy specimens were taken 72 h after the last irradiation. The amount of CPDs and the extent of apoptosis were measured by ELISA. Photolyase plus SS was superior to SS alone in reducing both the formation of CPDs and apoptotic cell death (both P<0.001). In conclusion, the addition of photolyase to a traditional SS contributes significantly to the prevention of UVR-induced DNA damage and apoptosis when applied topically to human skin.

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Ultraviolet radiation-induced apoptosis in keratinocytes: On the role of cytosolic factors

Cited by 145 publications

References 128 publications

The nucleotide excision repair pathway is required for UV-C-induced apoptosis in Caenorhabditis elegans

The nucleotide excision repair pathway is required for UV-C-induced apoptosis in Caenorhabditis elegans

Modulation of the UV-B-induced Oxidative Stress and Apoptosis in HaCaT Cell Line with <i>Calluna vulgaris</i> Extract

Reduced ultraviolet-induced DNA damage and apoptosis in human skin with topical application of a photolyase-containing DNA repair enzyme cream: Clues to skin cancer prevention

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