Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.

UVB radiation causes about 90% of non-melanoma skin cancers by damaging DNA either directly or indirectly by increasing levels of reactive oxygen species (ROS). Skin, chronically exposed to both endogenous and environmental pro-oxidant agents, contains a well-organised system of chemical and enzymat...

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Autores principales: Nicoletta Vitale, Annamaria Kisslinger, Simona Paladino, Claudio Procaccini, Giuseppe Matarese, Giovanna Maria Pierantoni, Francesco Paolo Mancini, Donatella Tramontano
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/b30bce4e93264644a389cf53cd7ad336
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spelling oai:doaj.org-article:b30bce4e93264644a389cf53cd7ad3362021-11-18T08:45:44ZResveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.1932-620310.1371/journal.pone.0080728https://doaj.org/article/b30bce4e93264644a389cf53cd7ad3362013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24260465/?tool=EBIhttps://doaj.org/toc/1932-6203UVB radiation causes about 90% of non-melanoma skin cancers by damaging DNA either directly or indirectly by increasing levels of reactive oxygen species (ROS). Skin, chronically exposed to both endogenous and environmental pro-oxidant agents, contains a well-organised system of chemical and enzymatic antioxidants. However, increased or prolonged free radical action can overwhelm ROS defence mechanisms, contributing to the development of cutaneous diseases. Thus, new strategies for skin protection comprise the use of food antioxidants to counteract oxidative stress. Resveratrol, a phytoalexin from grape, has gained a great interest for its ability to influence several biological mechanisms like redox balance, cell proliferation, signal transduction pathways, immune and inflammatory response. Therefore, the potential of resveratrol to modify skin cell response to UVB exposure could turn out to be a useful option to protect skin from sunlight-induced degenerative diseases. To investigate into this matter, HaCaT cells, a largely used model for human skin keratinocytes, were treated with 25 or 100 µM resveratrol for 2 and 24 hours prior to UVB irradiation (10 to 100 mJ/cm(2)). Cell viability and molecular markers of proliferation, oxidative stress, apoptosis, and autophagy were analyzed. In HaCaT cells resveratrol pretreatment: reduces UVB-induced ROS formation, enhances the detrimental effect of UVB on HaCaT cell vitality, increases UVB-induced caspase 8, PARP cleavage, and induces autophagy. These findings suggest that resveratrol could exert photochemopreventive effects by enhancing UVB-induced apoptosis and by inducing autophagy, thus reducing the odds that damaged cells could escape programmed cell death and initiate malignant transformation.Nicoletta VitaleAnnamaria KisslingerSimona PaladinoClaudio ProcacciniGiuseppe MatareseGiovanna Maria PierantoniFrancesco Paolo ManciniDonatella TramontanoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 11, p e80728 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Nicoletta Vitale
Annamaria Kisslinger
Simona Paladino
Claudio Procaccini
Giuseppe Matarese
Giovanna Maria Pierantoni
Francesco Paolo Mancini
Donatella Tramontano
Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.
description UVB radiation causes about 90% of non-melanoma skin cancers by damaging DNA either directly or indirectly by increasing levels of reactive oxygen species (ROS). Skin, chronically exposed to both endogenous and environmental pro-oxidant agents, contains a well-organised system of chemical and enzymatic antioxidants. However, increased or prolonged free radical action can overwhelm ROS defence mechanisms, contributing to the development of cutaneous diseases. Thus, new strategies for skin protection comprise the use of food antioxidants to counteract oxidative stress. Resveratrol, a phytoalexin from grape, has gained a great interest for its ability to influence several biological mechanisms like redox balance, cell proliferation, signal transduction pathways, immune and inflammatory response. Therefore, the potential of resveratrol to modify skin cell response to UVB exposure could turn out to be a useful option to protect skin from sunlight-induced degenerative diseases. To investigate into this matter, HaCaT cells, a largely used model for human skin keratinocytes, were treated with 25 or 100 µM resveratrol for 2 and 24 hours prior to UVB irradiation (10 to 100 mJ/cm(2)). Cell viability and molecular markers of proliferation, oxidative stress, apoptosis, and autophagy were analyzed. In HaCaT cells resveratrol pretreatment: reduces UVB-induced ROS formation, enhances the detrimental effect of UVB on HaCaT cell vitality, increases UVB-induced caspase 8, PARP cleavage, and induces autophagy. These findings suggest that resveratrol could exert photochemopreventive effects by enhancing UVB-induced apoptosis and by inducing autophagy, thus reducing the odds that damaged cells could escape programmed cell death and initiate malignant transformation.
format article
author Nicoletta Vitale
Annamaria Kisslinger
Simona Paladino
Claudio Procaccini
Giuseppe Matarese
Giovanna Maria Pierantoni
Francesco Paolo Mancini
Donatella Tramontano
author_facet Nicoletta Vitale
Annamaria Kisslinger
Simona Paladino
Claudio Procaccini
Giuseppe Matarese
Giovanna Maria Pierantoni
Francesco Paolo Mancini
Donatella Tramontano
author_sort Nicoletta Vitale
title Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.
title_short Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.
title_full Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.
title_fullStr Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.
title_full_unstemmed Resveratrol couples apoptosis with autophagy in UVB-irradiated HaCaT cells.
title_sort resveratrol couples apoptosis with autophagy in uvb-irradiated hacat cells.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/b30bce4e93264644a389cf53cd7ad336
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